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Molecular Medicine |
From the Departments of Molecular Physiology and Biological Physics (T.Y., S.S., F.D., B.R.W., M.H.H., G.K.O.) and Microbiology (B.E.K.), University of Virginia, Charlottesville, Va; and the Department of Molecular Biology (D.-Z.W., E.N.O.), University of Texas Southwestern Medical Center, Dallas, Tex.
Correspondence to Gary K. Owens, PhD, Department of Molecular Physiology and Biological Physics, University of Virginia, PO Box 800736, Charlottesville, VA 22908-0736. E-mail gko{at}virginia.edu
| Abstract |
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-actin, SM-myosin heavy chain, and SM22
by 9- to 60-fold in a CArG-dependent manner, whereas myocardin short interfering RNA markedly decreased activity of these promoters. Moreover, adenovirus-mediated overexpression of a dominant-negative form of myocardin significantly suppressed expression of endogenous SMC marker genes, whereas adenovirus-mediated overexpression of wild-type myocardin increased expression. Taken together, results provide compelling evidence that myocardin plays a key role as a transcriptional coactivator of SMC marker genes through CArG-dependent mechanisms.
Key Words: smooth muscle cells transcriptional coactivator serum response factor CArG element
| Introduction |
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Smooth muscle (SM)
-actin, SM-myosin heavy chain (MHC), and SM22
are useful markers for studying the control of SMC differentiation.2 Their expression levels are high in differentiated medial SMCs, whereas they are low in dedifferentiated intimal SMCs.2 These SMC-selective genes have a conserved DNA recognition element known as a CArG element, which has the general sequence motif, CC(A/T-rich)6GG.3 The CArG element was first identified as the core sequence of the serum response element (SRE) within the early-response gene, c-fos.3 Whereas there is only one SRE/CArG element in the c-fos gene, each of the SMC marker genes contains at least two CArG elements located in the 5' promoter region and the first intron.47 Previous studies from our laboratory and others have demonstrated that multiple CArG elements are required for SMC marker expression in vivo.6,8,9 The binding factor for CArG elements is the MADS box transcription factor, serum response factor (SRF).10 Although SRF is expressed in a wide variety of cells and controls gene expression in response to growth and differentiation signals, Landerholm et al11 have shown that SRF is required for differentiation of SMCs in an in vitro proepicardial cell model of coronary SMC differentiation. Our laboratory also recently showed that in SMCs, SRF is bound to CArG-containing regions in multiple SMC marker genes within intact chromatin.12
Despite overwhelming evidence indicating that CArG-SRF interactions are critical for expression of virtually all SMC-specific/-selective differentiation marker genes, the mechanisms by which a ubiquitously expressed transcription factor, SRF, contributes to SMC-specific/-selective expression are poorly understood. However, studies in our laboratory and by others have implicated some combination of the following factors and mechanisms: (1) cooperative interaction of multiple CArG elements including requirements regarding their spacing and phasing13; (2) combinatorial interaction with other cis-acting elements and their binding factors14,15; (3) regulation of SRF binding by homeodomain proteins such as MHox16; (4) possible translocation of SRF from cytoplasm to nucleus17; (5) selective regulation of SRF binding to CArG regions of SMC genes within intact chromatin12; and (6) recruitment of SRF accessory proteins that may be selective for SMCs.13 The latter mechanism is particularly interesting and was based on our observations of a unique SMC-selective CArG-SRF higher order complex in electrophoretic mobility shift assays (EMSAs).13 Of interest, formation of this higher order CArG-SRF complex was not dependent on CArG flanking sequences, but rather appeared to occur through protein-protein interactions and was observed with SMC nuclear extracts but not with extracts from a variety of other cell types. These results suggested the existence of SMC-selective SRF cofactors that may be important for controlling CArG-SRFdependent gene transcription in SMCs. However, a SMC-selective coactivator for SRF has not been identified yet.
Recently, Wang et al18 reported the cloning of a cDNA encoding a protein termed myocardin that is highly expressed in the heart and acts as a potent transcriptional coactivator for SRF. They found that myocardin directly bound to SRF and transactivated SM22
and atrial natriuretic factor promoter-reporter genes in COS cells via a CArG-dependent manner. They also demonstrated that myocardin was required for cardiomyocyte differentiation in vivo based on the overexpression of dominant-negative myocardin mutant in Xenopus embryos. Chen et al19 recently presented evidence that myocardin is also expressed in the aorta and can induce activation of several SMC marker genes in transfection studies. However, as yet, no studies have directly addressed whether myocardin normally plays a role in CArG-SRFdependent transcription of SMC marker genes. Thus, the goal of present studies was to investigate the role of myocardin in control of expression of SMC differentiation marker genes through a combination of loss and gain of function experiments in cultured SMCs and inducible SMC linage systems.
| Materials and Methods |
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RNA Extraction and Reverse Transcription (RT)-PCR
Total RNA was prepared from the tissues of adult female C57BL/6 mice (Harlan, Indianapolis, Ind) and cultured cells. The animal protocol was reviewed and approved by the animal care and use committee at the University of Virginia. Semiquantitative RT-PCR was performed as described previously.12
Construction of Reporter Plasmids
Myocardin expression plasmid and its carboxy-terminal truncation mutant, MyoC
381, were described previously.18 The fragments of rat SM
-actin (-2555 to +2813 bp),8 rat SM-MHC (-4220 to
+11600 bp),21 and mouse SM22
(-447 to +89 bp)22 were subcloned into a pGL3-basic vector (Promega Corp). Single CArG mutants of the SM
-actin gene were constructed by replacing the BstEII-AatII fragment with that of p2600Int/LacZ mutants.8 Double and triple CArG mutants were constructed using site-directed mutagenesis. A series of CArG flanking mutations in the p
A125Luc construct were made by inserting a HindIII-XbaI fragment of p125CAT mutation constructs13 into the pGL3-basic vector.
Construction of Short Interfering (si) RNA Plasmids
A plasmid-based system for production of siRNA was developed by ligating the minimal mouse H1 promoter (CCATGCAAATTACGC- TGTGCTTTGTGGGAAATCACCCTAAACGTAAAATTTATTCCTC- TTTCGAGCCTTATAGTGGCGGCCGGTCTACACCTTAAGGCGA) into the SacI-SpeI sites of pBluescript KS (-) (Stratagene), and this vector was named as pMighty-Empty. This system was tested for efficacy in SMCs, by successful knockdown of cotransfected green fluorescent protein (GFP) with pMighty-
GFP, which was constructed by inserting the oligonucleotide specific for GFP downstream of H1 promoter. To generate the siRNA specific for myocardin, an oligonucleotide (TTAAAGTTC- CGATCAGTCTTACAGTTCAAGAGACTGTAAGACTGATCGGA- ACTTTTTGGAAAG; italic means specific sequence to rat myocardin) was inserted downstream of H1 promoter, and it was designated as pMighty-
Myo.
Transient Transfection and Luciferase Assay
Approximately 24 hours before transfection, rat aortic SMCs were seeded at 1.5x104 cells/cm2 onto 12-well plates. Cells were transfected with plasmids using Superfect (Qiagen Inc). The total amount of DNA per well was kept constant by adding the corresponding amount of expression vector without a cDNA insert. Luciferase activity was measured and normalized by cellular protein concentrations. Each sample was examined in duplicate and it was repeated in 3 different experiments.
Adenovirus Constructs and Infection
Replication-deficient adenoviruses encoding the flag-tagged myocardin (Ad/Myo) and MyoC
381 (Ad/MyoDN) gene expressed from the CMV promoter were generated using standard methods by the University of Iowa Gene Transfer Vector Core.23 Twenty-four hours after plating, SMCs and ECs were infected with purified viruses for 1 hour at a multiplicity of infection (MOI) of 50, which infected greater than 95% of SMCs as defined by using GFP-expressing adenovirus.
Electrophoretic Mobility Shift Assay
Nuclear extracts were prepared from cultured rat aortic SMCs and bovine aortic ECs that were infected with Ad/Myo or empty adenovirus (Ad/Emp). EMSA were performed as previously described.13,20
Immunofluorescence
Rat aortic SMCs were seeded at 0.2x104 cells/cm2 on the day before transfection. SMCs were transfected with the myocardin or MyoC
381 expression plasmid and incubated for 72 hours. SMCs were fixed, permeabilized, and incubated with polyclonal anti-flag antibody (Sigma Chemical Co) and monoclonal anti-SM
-actin antibody (Sigma Chemical Co). Specific staining was detected with Cy2-conjugated anti-rabbit IgG antibody and Cy3-conjugated anti-mouse IgG antibody (Jackson ImmunoResearch Laboratories, Inc). Cells were counterstained with 4', 6-diamidino-2-phenylindole (DAPI).
Real-Time RT-PCR
To quantify the expression of mRNA in Ad/Myo- or Ad/Emp-infected SMCs, real-time RT-PCR analysis (iCycler, Bio-Rad Laboratories, Inc) was performed using either SYBR green (SM
-actin) or a dual fluorescencelabeled probe (SM-MHC and 18S rRNA).
An expanded Materials and Methods section can be found in the online data supplement available at http://www.circresaha.org.
| Results |
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Myocardin Induced Expression of Multiple SMC Marker Genes in Embryonic Fibroblasts and Cultured SMCs
To determine whether myocardin was capable of inducing expression of SMC differentiation marker genes, a myocardin expression vector was transfected into 10T1/2 cells and effects on expression of SMC marker genes examined by RT-PCR. Expression of SM
-actin and SM-MHC mRNA was substantially induced by myocardin in 10T1/2 cells (Figure 2A). Myocardin also activated the transcription of the SM
-actin, SM-MHC, and SM22
promoter-enhancer luciferase genes by 40-, 60-, and 9-fold, respectively, in cotransfection studies in SMCs (Figure 2B). Importantly, the SM
-actin and SM-MHC promoter-enhancer constructs tested are sufficient to drive expression in SMCs in vivo in transgenic mice in a manner that recapitulates that of the endogenous gene.8,21 Taken together, results demonstrate that overexpression of myocardin alone is sufficient to activate multiple SMC marker genes including the definitive marker SM-MHC in multipotential 10T1/2 cells and SMCs.
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Myocardin Was Included in SMC-Selective CArG-SRF Higher Order Complex in EMSA
Results of our previous studies provided evidence for formation of a unique SMC-selective CArG-SRF higher order complex using SMC nuclear extracts and 95-bp oligonucleotide probe containing CArGs B and A of the SM
-actin promoter.13 To determine whether myocardin was included in this complex, a series of EMSA were performed using nuclear extracts prepared from SMCs infected with an adenovirus expressing flag-tagged myocardin, because as yet, no specific antibodies are available to detect myocardin itself. As previously reported,13 we found evidence of a SMC-selective CArG-SRF complex using the 95-bp probe and SMC nuclear extracts (Figure 3, band B), that had lower mobility than the complex formed by the 95-bp probe and nuclear extracts from ECs (band A). Of major interest, the SMC-selective shift complex was supershifted by either an anti-SRF antibody or an anti-flag antibody. These results indicate that myocardin is a component of a SMC-selective CArG-SRF higher order complex within the context of SMC nuclear extracts.
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Either Two CArG Elements or CArG B Was Required for SM
-Actin Gene Transcription by Myocardin
To determine the importance of CArG elements in myocardin-induced SM
-actin gene transcription, we tested the effects of myocardin on activity of a series of promoter constructs containing mutations of either a single or combinations of each of three CArG elements located within the -2.6/+2.8 kb SM
-actin promoter-enhancer. Myocardin increased SM
-actin gene transcription in a dose-dependent manner (Figure 4A). Single CArG mutations of CArG B, CArG A, or the intronic CArG did not affect SM
-actin gene transactivation by myocardin. However, myocardin-induced transcription was markedly decreased in double or triple CArG mutants except p
A (-2.6/+2.8) CArG A+int mutation construct, which exhibited lower basal activity than wild-type, but which responded to myocardin similarly to wild-type (Figure 4B). These mutants responded to TGF-ß1 (data not shown), suggesting the lack of responsiveness was not due to loss of basal promoter activity. Results indicate that either two CArG elements or single CArG B is required for SM
-actin gene activation by myocardin.
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CArG Flanking Sequences Were Not Necessary for the SM
-Actin Gene Transactivation by Myocardin
Several reports have shown that the activity and specificity of CArG-dependent genes were regulated by CArG flanking sequences.13,14 To investigate the involvement of the sequences surrounding SM
-actin CArGs B and A in myocardin-induced transactivation, we tested a series of mutations in CArG flanking regions of the p
A125Luc construct (Figure 5A). Mutations used in this study were the same as those used in our previous study.13
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Myocardin activated transcription of the p
A125Luc construct by 124-fold in cultured SMCs (Figure 5B). Mutation of CArG B or double mutations of CArGs B and A completely abolished the response to myocardin. In contrast, all CArG flanking region mutants and the CArG A mutation construct exhibited over 10-fold increases by myocardin (Figures 5B and 5C). Our interpretation of these results is that sequences that flank the CArG elements are not necessary for the induction of the SM
-actin promoter by myocardin and that the basal SM
-actin promoter from -56 to +23 bp plus CArG B are sufficient to confer myocardin responsiveness.
siRNA Specific for Myocardin Decreased Transcriptional Activity of SMC Marker Genes in Aortic SMCs
Studies thus far have clearly shown that myocardin potently activates CArG-dependent transcription of SMC marker genes in cultured cells. To determine whether endogenous myocardin, which is expressed in our cultured SMCs (Figure 1B), regulates SMC marker gene expression, the effect of an siRNA specific for myocardin was examined by a plasmid-based siRNA production system. Aortic SMCs were cotransfected with SMC-selective marker promoter-enhancer reporter constructs and pMighty-
Myo, and luciferase activity measured. The siRNA specific for myocardin significantly decreased transcriptional activity of each SMC marker gene (Figure 6). Of interest, the myocardin siRNA reduced activity of SM
-actin and SM-MHC by 65% and 75%, respectively, but SM22
by only 40%. This result suggests that the contribution of myocardin may differ between SMC marker genes. However, the decreased efficacy in reducing SM22
may also be a function of this representing a truncated promoter that does not fully recapitulate expression of the endogenous SM22
gene,9 as is the case with SM
-actin8 and SM-MHC.21
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Wild-Type Myocardin Increased, Whereas the Dominant-Negative Myocardin, MyoC
381, Decreased Expression of Endogenous SMC Markers in Aortic SMCs
To further investigate the role of myocardin in SMC differentiation, the effects of myocardin and its dominant-negative form on endogenous SMC marker expression were examined. We used a carboxy-terminal deletion mutant of myocardin, MyoC
381, because it behaved as a dominant-negative manner in cotransfection studies with SM
-actin promoter-reporter constructs (online Figure 1, available in the online data supplement at http://www.circresaha.org). Aortic SMCs were transfected with flag-tagged MyoC
381 or flag-tagged myocardin, incubated for 72 hours, and used for immunofluorescence studies. Studies were performed in subconfluent cultures of SMCs leading to sub-optimal transfection efficiencies, for two reasons: (1) to permit dual immunofluorescence analyses of individual cells; and (2) because this is known to result in suboptimal expression of SMC differentiation markers, thereby permitting analyses of both repression and activation of differentiation. As shown in Figures 7A through 7D, expression of SM
-actin was markedly suppressed in the flag-tagged MyoC
381-expressing cells. Indeed, the fraction of MyoC
381-expressing cells that were positive for SM
-actin was only 10% as compared with 57% in non-MyoC
381-expressing cells in the same culture dish (online Table 2). In contrast, expression of SM
-actin protein was enhanced in flag-tagged myocardin-expressing cells (Figures 7E through 7H) with 83% of positive staining for SM
-actin compared with 54% in nonflag-tagged myocardin-expressing cells. GFP expression vector was used as a control, with no effect on the ratio of SM
-actinpositive cells.
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To further assess effects of myocardin and its dominant-negative form on expression of endogenous SMC marker genes, cultured SMCs were infected with either Ad/Myo or Ad/MyoDN and expression of SM
-actin and SM-MHC mRNA analyzed by real-time RT-PCR. Results showed that wild-type myocardin induced SM
-actin and SM-MHC mRNA expression significantly, whereas MyoC
381 suppressed expression (Figure 8). These results provide strong evidence that endogenous myocardin plays an important role in regulating expression of multiple SMC marker genes in SMCs.
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| Discussion |
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Results of the present studies confirm and extend previous studies of Wang et al18 who suggested that cooperative interaction of multiple CArG elements were necessary for myocardin-induced gene activation based on observations that myocardin induced the activity of a reporter construct containing 4 tandem copies of c-fos SRE linked to the E1b promoter, but not the single CArG containing c-fos gene construct in COS cells. In general, our results are consistent with their findings in that myocardin responsiveness was without question CArG-dependent. However, our results revealed a subtle but potentially significant difference in that we found that retention of a single CArG B element within the context of the -2.6/+2.8 kb SM
-actin promoter8 was sufficient to confer myocardin responsiveness. Although the underlying mechanisms responsible for this are unclear, results clearly indicate that gene context plays a critical role in determining myocardin responsiveness, perhaps through cooperative interaction with other cis- and trans-factors in a manner similar to myocyte enhancer factor-2 (MEF2), MyoD/myogenin, and SRF in skeletal muscle,25 where retention of only a subset of cis-elements for these factors was necessary for recruitment of other factors through protein-protein interactions. Consistent with this, results of the present studies provided evidence for formation of a higher order CArG-SRF-myocardin complex in SMCs that exhibited a lower mobility in EMSA than the equivalent complex in ECs. Although somewhat speculative, it is interesting to suggest that this may reflect recruitment of some additional factor(s) present in SMCs that is lacking in ECs. Indeed, we have previously published evidence for the existence of SMC-selective higher order CArG-SRF complex that was dependent on protein-protein interaction with CArG-SRF and not additional DNA sequences.13 However, much further investigation will be needed to reconcile these observations.
A particularly intriguing and potentially significant observation in the present studies was that myocardin mRNA was expressed in a novel A404 SMC precursor line, which we have previously described,12 but not in the P19 stem cells from which they were derived. Importantly, these SMC precursor cells do not express any known SMC marker gene.12 These observations have several possible important implications. First, myocardin may serve as a novel marker to identify SMC progenitor cells, although further in vivo studies will be necessary to test this possibility. Second, results indicate that, at least within some cell contexts, expression of myocardin alone is not sufficient to induce SMC differentiation. This is not surprising in that A404 cells may lack important cofactors or signals necessary for SMC gene activation. Indeed, we previously demonstrated that SRF could not bind to the CArG-containing regions of SMC marker genes within the context of intact chromatin, although SRF was able to bind to the CArG region of the c-fos gene in A404 cells.12 However, on RA treatment, cells exhibited a number of histone modifications consistent with chromatin relaxation and SRF bound to CArG regions of SMC marker genes. Taken together, results support a model in which A404 cells fail to activate SMC differentiation marker genes due to aspects of chromatin structure that prevent binding of SRF to CArG regions of SMC marker genes and subsequent recruitment of myocardin and/or other cofactors. Alternatively, because RA increased myocardin mRNA expression, it is possible that the level of expression of myocardin is simply insufficient to activate SMC marker genes in A404 cells. Of interest, myocardin has a SAP domain, named for scaffold attachment factors A and B (SAF-A/B), acinus, and protein inhibitor of activated STAT (PIAS), which may serve as a potential DNA-binding motif that could perform a specific role in chromatin organization.27 It is interesting to speculate that myocardin may elicit its effects, at least in part, by regulating chromatin structure. In any case, further studies are needed to identify what factors are induced by RA treatment in A404 cells that result in chromatin remodeling and coordinate activation of virtually all known SMC marker genes.
Although results of the present studies clearly implicate an important role for myocardin in the control of CArG-dependent SMC marker genes, it is clearly not a SMC-specific gene in that it is also expressed in cardiomyocytes. Of interest, many similarities exist in mechanisms that contribute to cell-specific gene expression in these two cell types beyond a dominant role of CArG-SRFdependent mechanisms.15,16,22,2832 For example, cell-specific expression in both cell types is believed to result from complex combinatorial interactions of multiple cis-acting elements and their trans-acting factors, none of which are completely cell-specific. Indeed, several gene families have been implicated in regulation of cell-specific expression in both cardiomyocytes and SMCs, including homeodomain proteins such as MHox and Nkx factors,16,28 GATA proteins,15,29 the Sp1 family,22,29 basic helix-loop-helix transcription factors,30,31 and the MEF-2 family.29,32 However, the precise mechanisms whereby these various factors act in concert with myocardin to regulate the complex temporal and spatial pattern of expression of various cardiac and SMC-specific genes remain to be elucidated. Identification of the cooperative mechanisms by which these transcription factors and their cofactors, including SRF and myocardin regulate SMC-specific expression will provide important insights regarding the control of differentiation and dedifferentiation of SMCs.
In summary, the results of the present studies implicate a critical role for myocardin in normal regulation of expression of multiple CArG-SRFdependent SMC marker genes in cultured cell systems. Moreover, our results and others18,19 show that myocardin is expressed both during early embryonic development as well as in adult SMCs. Although potentially of major significance, clearly further studies are needed to directly investigate the role of myocardin in vivo during development and after vascular injury that is characterized by phenotypic modulation of SMCs.22
| Acknowledgments |
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Received September 19, 2002; revision received February 25, 2003; accepted March 13, 2003.
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B. N. Davis, A. C. Hilyard, P. H. Nguyen, G. Lagna, and A. Hata Induction of MicroRNA-221 by Platelet-derived Growth Factor Signaling Is Critical for Modulation of Vascular Smooth Muscle Phenotype J. Biol. Chem., February 6, 2009; 284(6): 3728 - 3738. [Abstract] [Full Text] [PDF] |
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A. W. Orr, M. Y. Lee, J. A. Lemmon, A. Yurdagul Jr, M. F. Gomez, P. D. Schoppee Bortz, and B. R. Wamhoff Molecular Mechanisms of Collagen Isotype-Specific Modulation of Smooth Muscle Cell Phenotype Arterioscler Thromb Vasc Biol, February 1, 2009; 29(2): 225 - 231. [Abstract] [Full Text] [PDF] |
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L. Jin, T. Yoshida, R. Ho, G. K. Owens, and A. V. Somlyo The Actin-associated Protein Palladin Is Required for Development of Normal Contractile Properties of Smooth Muscle Cells Derived from Embryoid Bodies J. Biol. Chem., January 23, 2009; 284(4): 2121 - 2130. [Abstract] [Full Text] [PDF] |
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K. Kawai-Kowase, T. Ohshima, H. Matsui, T. Tanaka, T. Shimizu, T. Iso, M. Arai, G. K. Owens, and M. Kurabayashi PIAS1 Mediates TGF{beta}-Induced SM {alpha}-Actin Gene Expression Through Inhibition of KLF4 Function-Expression by Protein Sumoylation Arterioscler Thromb Vasc Biol, January 1, 2009; 29(1): 99 - 106. [Abstract] [Full Text] [PDF] |
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D. Morrow, S. Guha, C. Sweeney, Y. Birney, T. Walshe, C. O'Brien, D. Walls, E. M. Redmond, and P. A. Cahill Notch and Vascular Smooth Muscle Cell Phenotype Circ. Res., December 5, 2008; 103(12): 1370 - 1382. [Abstract] [Full Text] [PDF] |
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J. A. Lemmon and B. R. Wamhoff "FRNKly, Smooth Muscle, I Don't Give a CArG!": A Novel Mechanism for Smooth Muscle Cell Differentiation Arterioscler Thromb Vasc Biol, December 1, 2008; 28(12): 2091 - 2093. [Full Text] [PDF] |
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K. Vaahtomeri, E. Ventela, K. Laajanen, P. Katajisto, P.-J. Wipff, B. Hinz, T. Vallenius, M. Tiainen, and T. P. Makela Lkb1 is required for TGF{beta}-mediated myofibroblast differentiation J. Cell Sci., November 1, 2008; 121(21): 3531 - 3540. [Abstract] [Full Text] [PDF] |
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T. Yoshida, Q. Gan, and G. K. Owens Kruppel-like factor 4, Elk-1, and histone deacetylases cooperatively suppress smooth muscle cell differentiation markers in response to oxidized phospholipids Am J Physiol Cell Physiol, November 1, 2008; 295(5): C1175 - C1182. [Abstract] [Full Text] [PDF] |
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Y. Shang, T. Yoshida, B. A. Amendt, J. F. Martin, and G. K. Owens Pitx2 is functionally important in the early stages of vascular smooth muscle cell differentiation J. Cell Biol., October 14, 2008; 181(3): 461 - 473. [Abstract] [Full Text] [PDF] |
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M. A. Saleem, J. Zavadil, M. Bailly, K. McGee, I. R. Witherden, H. Pavenstadt, H. Hsu, J. Sanday, S. C. Satchell, R. Lennon, et al. The molecular and functional phenotype of glomerular podocytes reveals key features of contractile smooth muscle cells Am J Physiol Renal Physiol, October 1, 2008; 295(4): F959 - F970. [Abstract] [Full Text] [PDF] |
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P. E. Westerweel and M. C. Verhaar Directing Myogenic Mesenchymal Stem Cell Differentiation Circ. Res., September 12, 2008; 103(6): 560 - 561. [Full Text] [PDF] |
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E. S. Jeon, W. S. Park, M. J. Lee, Y. M. Kim, J. Han, and J. H. Kim A Rho Kinase/Myocardin-Related Transcription Factor-A-Dependent Mechanism Underlies the Sphingosylphosphorylcholine-Induced Differentiation of Mesenchymal Stem Cells Into Contractile Smooth Muscle Cells Circ. Res., September 12, 2008; 103(6): 635 - 642. [Abstract] [Full Text] [PDF] |
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M. S. Parmacek Myocardin: Dominant Driver of the Smooth Muscle Cell Contractile Phenotype Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1416 - 1417. [Full Text] [PDF] |
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X. Long, R. D. Bell, W. T. Gerthoffer, B. V. Zlokovic, and J. M. Miano Myocardin Is Sufficient for a Smooth Muscle-Like Contractile Phenotype Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1505 - 1510. [Abstract] [Full Text] [PDF] |
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B. R. Wamhoff, K. R. Lynch, T. L. Macdonald, and G. K. Owens Sphingosine-1-Phosphate Receptor Subtypes Differentially Regulate Smooth Muscle Cell Phenotype Arterioscler Thromb Vasc Biol, August 1, 2008; 28(8): 1454 - 1461. [Abstract] [Full Text] [PDF] |
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D.L. Tharp, B.R. Wamhoff, H. Wulff, G. Raman, A. Cheong, and D.K. Bowles Local Delivery of the KCa3.1 Blocker, TRAM-34, Prevents Acute Angioplasty-Induced Coronary Smooth Muscle Phenotypic Modulation and Limits Stenosis Arterioscler Thromb Vasc Biol, June 1, 2008; 28(6): 1084 - 1089. [Abstract] [Full Text] [PDF] |
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D.-W. Lin, I.-C. Chang, A. Tseng, M.-L. Wu, C.-H. Chen, C. A. Patenaude, M. D. Layne, and S.-F. Yet Transforming Growth Factor {beta} Up-regulates Cysteine-rich Protein 2 in Vascular Smooth Muscle Cells via Activating Transcription Factor 2 J. Biol. Chem., May 30, 2008; 283(22): 15003 - 15014. [Abstract] [Full Text] [PDF] |
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G. Elberg, L. Chen, D. Elberg, M. D. Chan, C. J. Logan, and M. A. Turman MKL1 mediates TGF-{beta}1-induced {alpha}-smooth muscle actin expression in human renal epithelial cells Am J Physiol Renal Physiol, May 1, 2008; 294(5): F1116 - F1128. [Abstract] [Full Text] [PDF] |
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P. Au, J. Tam, D. Fukumura, and R. K. Jain Bone marrow-derived mesenchymal stem cells facilitate engineering of long-lasting functional vasculature Blood, May 1, 2008; 111(9): 4551 - 4558. [Abstract] [Full Text] [PDF] |
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S. Kennard, H. Liu, and B. Lilly Transforming Growth Factor- (TGF- 1) Down-regulates Notch3 in Fibroblasts to Promote Smooth Muscle Gene Expression J. Biol. Chem., January 18, 2008; 283(3): 1324 - 1333. [Abstract] [Full Text] [PDF] |
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T. Zhang, S. Zhuang, D. E. Casteel, D. J. Looney, G. R. Boss, and R. B. Pilz A Cysteine-rich LIM-only Protein Mediates Regulation of Smooth Muscle-specific Gene Expression by cGMP-dependent Protein Kinase J. Biol. Chem., November 16, 2007; 282(46): 33367 - 33380. [Abstract] [Full Text] [PDF] |
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Q. Gan, T. Yoshida, J. Li, and G. K. Owens Smooth Muscle Cells and Myofibroblasts Use Distinct Transcriptional Mechanisms for Smooth Muscle {alpha}-Actin Expression Circ. Res., October 26, 2007; 101(9): 883 - 892. [Abstract] [Full Text] [PDF] |
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N. A. Pidkovka, O. A. Cherepanova, T. Yoshida, M. R. Alexander, R. A. Deaton, J. A. Thomas, N. Leitinger, and G. K. Owens Oxidized Phospholipids Induce Phenotypic Switching of Vascular Smooth Muscle Cells In Vivo and In Vitro Circ. Res., October 12, 2007; 101(8): 792 - 801. [Abstract] [Full Text] [PDF] |
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A. Kanematsu, A. Ramachandran, and R. M. Adam GATA-6 mediates human bladder smooth muscle differentiation: involvement of a novel enhancer element in regulating {alpha}-smooth muscle actin gene expression Am J Physiol Cell Physiol, September 1, 2007; 293(3): C1093 - C1102. [Abstract] [Full Text] [PDF] |
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M. Zhang, H. Fang, J. Zhou, and B. P. Herring A Novel Role of Brg1 in the Regulation of SRF/MRTFA-dependent Smooth Muscle-specific Gene Expression J. Biol. Chem., August 31, 2007; 282(35): 25708 - 25716. [Abstract] [Full Text] [PDF] |
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F. Li, Z. Luo, W. Huang, Q. Lu, C. S. Wilcox, P. A. Jose, and S. Chen Response Gene to Complement 32, a Novel Regulator for Transforming Growth Factor-beta-induced Smooth Muscle Differentiation of Neural Crest Cells J. Biol. Chem., April 6, 2007; 282(14): 10133 - 10137. [Abstract] [Full Text] [PDF] |
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M. S. Parmacek Myocardin-Related Transcription Factors: Critical Coactivators Regulating Cardiovascular Development and Adaptation Circ. Res., March 16, 2007; 100(5): 633 - 644. [Abstract] [Full Text] [PDF] |
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D. P. Staus, A. L. Blaker, J. M. Taylor, and C. P. Mack Diaphanous 1 and 2 Regulate Smooth Muscle Cell Differentiation by Activating the Myocardin-Related Transcription Factors Arterioscler Thromb Vasc Biol, March 1, 2007; 27(3): 478 - 486. [Abstract] [Full Text] [PDF] |
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K. Touw, A. M. Hoggatt, G. Simon, and B. P. Herring Hprt-targeted transgenes provide new insights into smooth muscle-restricted promoter activity Am J Physiol Cell Physiol, March 1, 2007; 292(3): C1024 - C1032. [Abstract] [Full Text] [PDF] |
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T. Yoshida, Q. Gan, Y. Shang, and G. K. Owens Platelet-derived growth factor-BB represses smooth muscle cell marker genes via changes in binding of MKL factors and histone deacetylases to their promoters Am J Physiol Cell Physiol, February 1, 2007; 292(2): C886 - C895. [Abstract] [Full Text] [PDF] |
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N. Chow, R. D. Bell, R. Deane, J. W. Streb, J. Chen, A. Brooks, W. Van Nostrand, J. M. Miano, and B. V. Zlokovic Serum response factor and myocardin mediate arterial hypercontractility and cerebral blood flow dysregulation in Alzheimer's phenotype PNAS, January 16, 2007; 104(3): 823 - 828. [Abstract] [Full Text] [PDF] |
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K. Kawai-Kowase and G. K. Owens Multiple repressor pathways contribute to phenotypic switching of vascular smooth muscle cells Am J Physiol Cell Physiol, January 1, 2007; 292(1): C59 - C69. [Abstract] [Full Text] [PDF] |
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E. S. Jeon, H. J. Moon, M. J. Lee, H. Y. Song, Y. M. Kim, Y. C. Bae, J. S. Jung, and J. H. Kim Sphingosylphosphorylcholine induces differentiation of human mesenchymal stem cells into smooth-muscle-like cells through a TGF-{beta}-dependent mechanism J. Cell Sci., December 1, 2006; 119(23): 4994 - 5005. [Abstract] [Full Text] [PDF] |
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B. P. Herring, O. El-Mounayri, P. J. Gallagher, F. Yin, and J. Zhou Regulation of myosin light chain kinase and telokin expression in smooth muscle tissues Am J Physiol Cell Physiol, November 1, 2006; 291(5): C817 - C827. [Abstract] [Full Text] [PDF] |
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E. E. Creemers, L. B. Sutherland, J. McAnally, J. A. Richardson, and E. N. Olson Myocardin is a direct transcriptional target of Mef2, Tead and Foxo proteins during cardiovascular development Development, November 1, 2006; 133(21): 4245 - 4256. [Abstract] [Full Text] [PDF] |
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D. L. Tharp, B. R. Wamhoff, J. R. Turk, and D. K. Bowles Upregulation of intermediate-conductance Ca2+-activated K+ channel (IKCa1) mediates phenotypic modulation of coronary smooth muscle Am J Physiol Heart Circ Physiol, November 1, 2006; 291(5): H2493 - H2503. [Abstract] [Full Text] [PDF] |
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H. Doi, T. Iso, H. Sato, M. Yamazaki, H. Matsui, T. Tanaka, I. Manabe, M. Arai, R. Nagai, and M. Kurabayashi Jagged1-selective Notch Signaling Induces Smooth Muscle Differentiation via a RBP-J{kappa}-dependent Pathway J. Biol. Chem., September 29, 2006; 281(39): 28555 - 28564. [Abstract] [Full Text] [PDF] |
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S. Li, S. Chang, X. Qi, J. A. Richardson, and E. N. Olson Requirement of a Myocardin-Related Transcription Factor for Development of Mammary Myoepithelial Cells Mol. Cell. Biol., August 1, 2006; 26(15): 5797 - 5808. [Abstract] [Full Text] [PDF] |
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Y. Sun, K. Boyd, W. Xu, J. Ma, C. W. Jackson, A. Fu, J. M. Shillingford, G. W. Robinson, L. Hennighausen, J. K. Hitzler, et al. Acute Myeloid Leukemia-Associated Mkl1 (Mrtf-a) Is a Key Regulator of Mammary Gland Function Mol. Cell. Biol., August 1, 2006; 26(15): 5809 - 5826. [Abstract] [Full Text] [PDF] |
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F. Yin, A. M. Hoggatt, J. Zhou, and B. P. Herring 130-kDa smooth muscle myosin light chain kinase is transcribed from a CArG-dependent, internal promoter within the mouse mylk gene Am J Physiol Cell Physiol, June 1, 2006; 290(6): C1599 - C1609. [Abstract] [Full Text] [PDF] |
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W. Xing, T.-C. Zhang, D. Cao, Z. Wang, C. L. Antos, S. Li, Y. Wang, E. N. Olson, and D.-Z. Wang Myocardin Induces Cardiomyocyte Hypertrophy Circ. Res., April 28, 2006; 98(8): 1089 - 1097. [Abstract] [Full Text] [PDF] |
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B. R. Wamhoff, D. K. Bowles, and G. K. Owens Excitation-Transcription Coupling in Arterial Smooth Muscle Circ. Res., April 14, 2006; 98(7): 868 - 878. [Abstract] [Full Text] [PDF] |
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S. S.M. Rensen, P. M.G. Niessen, X. Long, P. A. Doevendans, J. M. Miano, and G. J.J.M. van Eys Contribution of serum response factor and myocardin to transcriptional regulation of smoothelins Cardiovasc Res, April 1, 2006; 70(1): 136 - 145. [Abstract] [Full Text] [PDF] |
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I. Gorenne, L. Jin, T. Yoshida, J.M. Sanders, I.J. Sarembock, G.K. Owens, A.P. Somlyo, and A.V. Somlyo LPP Expression During In Vitro Smooth Muscle Differentiation and Stent-Induced Vascular Injury Circ. Res., February 17, 2006; 98(3): 378 - 385. [Abstract] [Full Text] [PDF] |
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J. Zhou, G. Hu, and B. P. Herring Smooth Muscle-Specific Genes Are Differentially Sensitive to Inhibition by Elk-1 Mol. Cell. Biol., November 15, 2005; 25(22): 9874 - 9885. [Abstract] [Full Text] [PDF] |
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T. E. Callis, D. Cao, and D.-Z. Wang Bone Morphogenetic Protein Signaling Modulates Myocardin Transactivation of Cardiac Genes Circ. Res., November 11, 2005; 97(10): 992 - 1000. [Abstract] [Full Text] [PDF] |
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P. Qiu, R. P. Ritchie, Z. Fu, D. Cao, J. Cumming, J. M. Miano, D.-Z. Wang, H. J. Li, and L. Li Myocardin Enhances Smad3-Mediated Transforming Growth Factor-{beta}1 Signaling in a CArG Box-Independent Manner: Smad-Binding Element Is an Important cis Element for SM22{alpha} Transcription In Vivo Circ. Res., November 11, 2005; 97(10): 983 - 991. [Abstract] [Full Text] [PDF] |
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H. Doi, T. Iso, M. Yamazaki, H. Akiyama, H. Kanai, H. Sato, K. Kawai-Kowase, T. Tanaka, T. Maeno, E.-i. Okamoto, et al. HERP1 Inhibits Myocardin-Induced Vascular Smooth Muscle Cell Differentiation by Interfering With SRF Binding to CArG Box Arterioscler Thromb Vasc Biol, November 1, 2005; 25(11): 2328 - 2334. [Abstract] [Full Text] [PDF] |
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J. Francis, S. K. Chakrabarti, J. C. Garmey, and R. G. Mirmira Pdx-1 Links Histone H3-Lys-4 Methylation to RNA Polymerase II Elongation during Activation of Insulin Transcription J. Biol. Chem., October 28, 2005; 280(43): 36244 - 36253. [Abstract] [Full Text] [PDF] |
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J. Oh, J. A. Richardson, and E. N. Olson Requirement of myocardin-related transcription factor-B for remodeling of branchial arch arteries and smooth muscle differentiation PNAS, October 18, 2005; 102(42): 15122 - 15127. [Abstract] [Full Text] [PDF] |
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K. Kawai-Kowase, M. S. Kumar, M. H. Hoofnagle, T. Yoshida, and G. K. Owens PIAS1 Activates the Expression of Smooth Muscle Cell Differentiation Marker Genes by Interacting with Serum Response Factor and Class I Basic Helix-Loop-Helix Proteins Mol. Cell. Biol., September 15, 2005; 25(18): 8009 - 8023. [Abstract] [Full Text] [PDF] |
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J. van Tuyn, S. Knaan-Shanzer, M. J.M. van de Watering, M. de Graaf, A. van der Laarse, M. J. Schalij, E. E. van der Wall, A. A.F. de Vries, and D. E. Atsma Activation of cardiac and smooth muscle-specific genes in primary human cells after forced expression of human myocardin Cardiovasc Res, August 1, 2005; 67(2): 245 - 255. [Abstract] [Full Text] [PDF] |
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L. V. G. Bosc, J. J. Layne, M. T. Nelson, and D. C. Hill-Eubanks Nuclear Factor of Activated T Cells and Serum Response Factor Cooperatively Regulate the Activity of an {alpha}-Actin Intronic Enhancer J. Biol. Chem., July 15, 2005; 280(28): 26113 - 26120. [Abstract] [Full Text] [PDF] |
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J. Zhou and B. P. Herring Mechanisms Responsible for the Promoter-specific Effects of Myocardin J. Biol. Chem., March 18, 2005; 280(11): 10861 - 10869. [Abstract] [Full Text] [PDF] |
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A. Proweller, W. S. Pear, and M. S. Parmacek Notch Signaling Represses Myocardin-induced Smooth Muscle Cell Differentiation J. Biol. Chem., March 11, 2005; 280(10): 8994 - 9004. [Abstract] [Full Text] [PDF] |
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Y. Liu, S. Sinha, O. G. McDonald, Y. Shang, M. H. Hoofnagle, and G. K. Owens Kruppel-like Factor 4 Abrogates Myocardin-induced Activation of Smooth Muscle Gene Expression J. Biol. Chem., March 11, 2005; 280(10): 9719 - 9727. [Abstract] [Full Text] [PDF] |
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E. M. Small, A. S. Warkman, D.-Z. Wang, L. B. Sutherland, E. N. Olson, and P. A. Krieg Myocardin is sufficient and necessary for cardiac gene expression in Xenopus Development, March 1, 2005; 132(5): 987 - 997. [Abstract] [Full Text] [PDF] |
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T. Yoshida and G. K. Owens Molecular Determinants of Vascular Smooth Muscle Cell Diversity Circ. Res., February 18, 2005; 96(3): 280 - 291. [Abstract] [Full Text] [PDF] |
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J. W. Streb and J. M. Miano AKAP12{alpha}, an Atypical Serum Response Factor-dependent Target Gene J. Biol. Chem., February 11, 2005; 280(6): 4125 - 4134. [Abstract] [Full Text] [PDF] |
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F. Yin and B. P. Herring GATA-6 Can Act as a Positive or Negative Regulator of Smooth Muscle-specific Gene Expression J. Biol. Chem., February 11, 2005; 280(6): 4745 - 4752. [Abstract] [Full Text] [PDF] |
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S. Drori, G. D. Girnun, L. Tou, J. D. Szwaya, E. Mueller, X. Kia, R. A. Shivdasani, and B. M. Spiegelman Hic-5 regulates an epithelial program mediated by PPAR{gamma} Genes & Dev., February 1, 2005; 19(3): 362 - 375. [Abstract] [Full Text] [PDF] |
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J. J. Lepore, T. P. Cappola, P. A. Mericko, E. E. Morrisey, and M. S. Parmacek GATA-6 Regulates Genes Promoting Synthetic Functions in Vascular Smooth Muscle Cells Arterioscler Thromb Vasc Biol, February 1, 2005; 25(2): 309 - 314. [Abstract] [Full Text] [PDF] |
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S. Li, M. P. Czubryt, J. McAnally, R. Bassel-Duby, J. A. Richardson, F. F. Wiebel, A. Nordheim, and E. N. Olson Requirement for serum response factor for skeletal muscle growth and maturation revealed by tissue-specific gene deletion in mice PNAS, January 25, 2005; 102(4): 1082 - 1087. [Abstract] [Full Text] [PDF] |
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D. Cao, Z. Wang, C.-L. Zhang, J. Oh, W. Xing, S. Li, J. A. Richardson, D.-Z. Wang, and E. N. Olson Modulation of Smooth Muscle Gene Expression by Association of Histone Acetyltransferases and Deacetylases with Myocardin Mol. Cell. Biol., January 1, 2005; 25(1): 364 - 376. [Abstract] [Full Text] [PDF] |
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J. M. Miano, N. Ramanan, M. A. Georger, K. L. de Mesy Bentley, R. L. Emerson, R. O. Balza Jr., Q. Xiao, H. Weiler, D. D. Ginty, and R. P. Misra Restricted inactivation of serum response factor to the cardiovascular system PNAS, December 7, 2004; 101(49): 17132 - 17137. [Abstract] [Full Text] [PDF] |
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S. Sinha, M. H. Hoofnagle, P. A. Kingston, M. E. McCanna, and G. K. Owens Transforming growth factor-{beta}1 signaling contributes to development of smooth muscle cells from embryonic stem cells Am J Physiol Cell Physiol, December 1, 2004; 287(6): C1560 - C1568. [Abstract] [Full Text] [PDF] |
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J. M. Spin, S. Nallamshetty, R. Tabibiazar, E. A. Ashley, J. Y. King, M. Chen, P. S. Tsao, and T. Quertermous Transcriptional profiling of in vitro smooth muscle cell differentiation identifies specific patterns of gene and pathway activation Physiol Genomics, November 17, 2004; 19(3): 292 - 302. [Abstract] [Full Text] [PDF] |
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B.R. Wamhoff, M.H. Hoofnagle, A. Burns, S. Sinha, O.G. McDonald, and G.K. Owens A G/C Element Mediates Repression of the SM22{alpha} Promoter Within Phenotypically Modulated Smooth Muscle Cells in Experimental Atherosclerosis Circ. Res., November 12, 2004; 95(10): 981 - 988. [Abstract] [Full Text] [PDF] |
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K. Lockman, J. S. Hinson, M. D. Medlin, D. Morris, J. M. Taylor, and C. P. Mack Sphingosine 1-Phosphate Stimulates Smooth Muscle Cell Differentiation and Proliferation by Activating Separate Serum Response Factor Co-factors J. Biol. Chem., October 8, 2004; 279(41): 42422 - 42430. [Abstract] [Full Text] [PDF] |
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J. Oh, Z. Wang, D.-Z. Wang, C.-L. Lien, W. Xing, and E. N. Olson Target Gene-Specific Modulation of Myocardin Activity by GATA Transcription Factors Mol. Cell. Biol., October 1, 2004; 24(19): 8519 - 8528. [Abstract] [Full Text] [PDF] |
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M. S. Parmacek Myocardin--Not Quite MyoD Arterioscler Thromb Vasc Biol, September 1, 2004; 24(9): 1535 - 1537. [Full Text] [PDF] |
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M. Takeji, N. Kawada, T. Moriyama, K. Nagatoya, S. Oseto, S. Akira, M. Hori, E. Imai, and T. Miwa CCAAT/Enhancer-Binding Protein {delta} Contributes to Myofibroblast Transdifferentiation and Renal Disease Progression J. Am. Soc. Nephrol., September 1, 2004; 15(9): 2383 - 2390. [Abstract] [Full Text] [PDF] |
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T. Yoshida, K. Kawai-Kowase, and G. K. Owens Forced Expression of Myocardin Is Not Sufficient for Induction of Smooth Muscle Differentiation in Multipotential Embryonic Cells Arterioscler Thromb Vasc Biol, September 1, 2004; 24(9): 1596 - 1601. [Abstract] [Full Text] [PDF] |
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P. R. Reynolds, M. L. Mucenski, T. D. Le Cras, W. C. Nichols, and J. A. Whitsett Midkine Is Regulated by Hypoxia and Causes Pulmonary Vascular Remodeling J. Biol. Chem., August 27, 2004; 279(35): 37124 - 37132. [Abstract] [Full Text] [PDF] |
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Z. Han, X. Li, J. Wu, and E. N. Olson A myocardin-related transcription factor regulates activity of serum response factor in Drosophila PNAS, August 24, 2004; 101(34): 12567 - 12572. [Abstract] [Full Text] [PDF] |
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J. M. Miano Channeling to Myocardin Circ. Res., August 20, 2004; 95(4): 340 - 342. [Full Text] [PDF] |
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B.R. Wamhoff, D.K. Bowles, O.G. McDonald, S. Sinha, A.P. Somlyo, A.V. Somlyo, and G.K. Owens L-type Voltage-Gated Ca2+ Channels Modulate Expression of Smooth Muscle Differentiation Marker Genes via a Rho Kinase/Myocardin/SRF-Dependent Mechanism Circ. Res., August 20, 2004; 95(4): 406 - 414. [Abstract] [Full Text] [PDF] |
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S. Albinsson, I. Nordstrom, and P. Hellstrand Stretch of the Vascular Wall Induces Smooth Muscle Differentiation by Promoting Actin Polymerization J. Biol. Chem., August 13, 2004; 279(33): 34849 - 34855. [Abstract] [Full Text] [PDF] |
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K. Kawai-Kowase, H. Sato, Y. Oyama, H. Kanai, M. Sato, H. Doi, and M. Kurabayashi Basic Fibroblast Growth Factor Antagonizes Transforming Growth Factor-{beta}1-Induced Smooth Muscle Gene Expression Through Extracellular Signal-Regulated Kinase 1/2 Signaling Pathway Activation Arterioscler Thromb Vasc Biol, August 1, 2004; 24(8): 1384 - 1390. [Abstract] [Full Text] [PDF] |
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G. K. Owens, M. S. Kumar, and B. R. Wamhoff Molecular Regulation of Vascular Smooth Muscle Cell Differentiation in Development and Disease Physiol Rev, July 1, 2004; 84(3): 767 - 801. [Abstract] [Full Text] [PDF] |
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S. Brunelli, E. Tagliafico, F. G. De Angelis, R. Tonlorenzi, S. Baesso, S. Ferrari, M. Niinobe, K. Yoshikawa, R. J. Schwartz, I. Bozzoni, et al. Msx2 and Necdin Combined Activities Are Required for Smooth Muscle Differentiation in Mesoangioblast Stem Cells Circ. Res., June 25, 2004; 94(12): 1571 - 1578. [Abstract] [Full Text] [PDF] |
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J. P. Anderson, E. Dodou, A. B. Heidt, S. J. De Val, E. J. Jaehnig, S. B. Greene, E. N. Olson, and B. L. Black HRC Is a Direct Transcriptional Target of MEF2 during Cardiac, Skeletal, and Arterial Smooth Muscle Development In Vivo Mol. Cell. Biol., May 1, 2004; 24(9): 3757 - 3768. [Abstract] [Full Text] [PDF] |
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T. Yoshida, M. H. Hoofnagle, and G. K. Owens Myocardin and Prx1 Contribute to Angiotensin II-Induced Expression of Smooth Muscle {alpha}-Actin Circ. Res., April 30, 2004; 94(8): 1075 - 1082. [Abstract] [Full Text] [PDF] |
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K. L. Du, M. Chen, J. Li, J. J. Lepore, P. Mericko, and M. S. Parmacek Megakaryoblastic Leukemia Factor-1 Transduces Cytoskeletal Signals and Induces Smooth Muscle Cell Differentiation from Undifferentiated Embryonic Stem Cells J. Biol. Chem., April 23, 2004; 279(17): 17578 - 17586. [Abstract] [Full Text] [PDF] |
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R. B. Pilz and D. E. Casteel Regulation of Gene Expression by Cyclic GMP Circ. Res., November 28, 2003; 93(11): 1034 - 1046. [Abstract] [Full Text] [PDF] |
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A. Selvaraj and R. Prywes Megakaryoblastic Leukemia-1/2, a Transcriptional Co-activator of Serum Response Factor, Is Required for Skeletal Myogenic Differentiation J. Biol. Chem., October 24, 2003; 278(43): 41977 - 41987. [Abstract] [Full Text] [PDF] |
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R. J. Kelm Jr., S.-X. Wang, J. A. Polikandriotis, and A. R. Strauch Structure/Function Analysis of Mouse Pur{beta}, a Single-stranded DNA-binding Repressor of Vascular Smooth Muscle {alpha}-Actin Gene Transcription J. Biol. Chem., October 3, 2003; 278(40): 38749 - 38757. [Abstract] [Full Text] [PDF] |
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E. N. Olson and M. D. Schneider Sizing up the heart: development redux in disease Genes & Dev., August 15, 2003; 17(16): 1937 - 1956. [Full Text] [PDF] |
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S. Li, D.-Z. Wang, Z. Wang, J. A. Richardson, and E. N. Olson The serum response factor coactivator myocardin is required for vascular smooth muscle development PNAS, August 5, 2003; 100(16): 9366 - 9370. [Abstract] [Full Text] [PDF] |
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Z. Wang, D.-Z. Wang, G. C. T. Pipes, and E. N. Olson Myocardin is a master regulator of smooth muscle gene expression PNAS, June 10, 2003; 100(12): 7129 - 7134. [Abstract] [Full Text] [PDF] |
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M. Beckman Rise to Power Sci. Aging Knowl. Environ., May 28, 2003; 2003(21): nw75 - 75. [Full Text] |
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M. W. Majesky Decisions, Decisions ... SRF Coactivators and Smooth Muscle Myogenesis Circ. Res., May 2, 2003; 92(8): 824 - 826. [Full Text] [PDF] |
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