© 1996 American Heart Association, Inc.
Articles |
Stress-Activated Protein Kinases in Cardiovascular Disease
From the Cardiac (T.F., C.M.P.), Renal (C.M.P., J.V.B.), and Diabetes (J.A.A., J.M.K.) Units of the Massachusetts General Hospital, Charlestown, and the Department of Medicine, Harvard Medical School, Boston, Mass.
Correspondence to Dr Thomas Force, Massachusetts General Hospital East, Suite 4002, 149 13th St, Charlestown, MA 02129.
Key Words: signal transduction • protein kinase • ischemia • stress • inflammatory cytokines
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Introduction |
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Cells respond to extracellular stimuli by activating signal transduction pathways, which culminate in changes in gene expression. The particular genetic program activated determines, in large part, the response of the cell (eg, growth versus growth arrest versus apoptosis; differentiation versus dedifferentiation). A critical component of eukaryotic signal transduction is the activation of protein kinases, which phosphorylate a host of cellular substrates, including transcription factors controlling the induction of various genes. For example, the Ras/ERK-1 and ERK-2 (or MAP kinase) pathway transduces critical components of the growth factor–induced mitogenic response to the nucleus. Expression of inactive or interfering mutants of components of the pathway disrupts, and expression of constitutively active mutants activates, mitogenesis.1
Recently, protein serine/threonine kinases related to ERK-1 and -2 have
been identified; these kinases transduce signals to the nucleus not in
response to growth factors and other mitogens but in response to
cellular stresses such as inflammatory cytokines (IL-1ß and
TNF-
), ischemia, reversible ATP depletion, heat shock,
endotoxin, and genotoxic stress. These kinases, called the
SAPKs2 or, alternatively, c-Jun N-terminal
(amino-terminal) kinases (JNKs, named after one of their
physiological substrates),3 and
p38,4 likely play critical roles in the genetic response
of many components of the cardiovascular system to
disease processes (Table
). In this review, we will
discuss these stress-activated kinases, how they are
regulated, and the evidence suggesting roles they may play in
cardiovascular disease.
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Stress-Activated Kinases |
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The SAPKs were first described in 1990 as the
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V. L. Gabai, A. B. Meriin, J. A. Yaglom, J. Y. Wei, D. D. Mosser, and M. Y. Sherman Suppression of Stress Kinase JNK Is Involved in HSP72-mediated Protection of Myogenic Cells from Transient Energy Deprivation. HSP72 ALLEVIATES THE STRESS-INDUCED INHIBITION OF JNK DEPHOSPHORYLATION J. Biol. Chem., November 22, 2000; 275(48): 38088 - 38094. [Abstract] [Full Text] [PDF]
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S. Eguchi, P. J. Dempsey, G. D. Frank, E. D. Motley, and T. Inagami Activation of MAPKs by Angiotensin II in Vascular Smooth Muscle Cells. METALLOPROTEASE-DEPENDENT EGF RECEPTOR ACTIVATION IS REQUIRED FOR ACTIVATION OF ERK AND p38 MAPK BUT NOT FOR JNK J. Biol. Chem., March 9, 2001; 276(11): 7957 - 7962. [Abstract] [Full Text] [PDF]
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U. Schmitz, K. Thommes, I. Beier, W. Wagner, A. Sachinidis, R. Dusing, and H. Vetter Angiotensin II-induced Stimulation of p21-activated Kinase and c-Jun NH2-terminal Kinase Is Mediated by Rac1 and Nck J. Biol. Chem., June 15, 2001; 276(25): 22003 - 22010. [Abstract] [Full Text] [PDF]
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A. Makkinje, D. A. Quinn, A. Chen, C. L. Cadilla, T. Force, J. V. Bonventre, and J. M. Kyriakis Gene 33/Mig-6, a Transcriptionally Inducible Adapter Protein That Binds GTP-Cdc42 and Activates SAPK/JNK. A POTENTIAL MARKER TRANSCRIPT FOR CHRONIC PATHOLOGIC CONDITIONS, SUCH AS DIABETIC NEPHROPATHY. POSSIBLE ROLE IN THE RESPONSE TO PERSISTENT STRESS J. Biol. Chem., June 2, 2000; 275(23): 17838 - 17847. [Abstract] [Full Text] [PDF]
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S. Murasawa, H. Matsubara, Y. Mori, H. Masaki, Y. Tsutsumi, Y. Shibasaki, I. Kitabayashi, Y. Tanaka, S. Fujiyama, Y. Koyama, et al. Angiotensin II Initiates Tyrosine Kinase Pyk2-dependent Signalings Leading to Activation of Rac1-mediated c-Jun NH2-terminal Kinase J. Biol. Chem., August 25, 2000; 275(35): 26856 - 26863. [Abstract] [Full Text] [PDF]
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Y. Izumi, S. Kim, M. Namba, H. Yasumoto, H. Miyazaki, M. Hoshiga, Y. Kaneda, R. Morishita, Y. Zhan, and H. Iwao Gene Transfer of Dominant-Negative Mutants of Extracellular Signal-Regulated Kinase and c-Jun NH2-Terminal Kinase Prevents Neointimal Formation in Balloon-Injured Rat Artery Circ. Res., June 8, 2001; 88(11): 1120 - 1126. [Abstract] [Full Text] [PDF]
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