doi: 10.1161/CIRCRESAHA.108.133333
© 2008 American Heart Association, Inc.
Correction
In the article by Chavakis et al, "Phosphatidylinositol-3-Kinase-
Is Integral to Homing Functions of Progenitor Cells," which appeared in the April 25, 2008 issue of the journal (Circ Res. 2008;102:942–949), the descriptions of the standard error (SE) and the standard error of the mean (SEM) were not included in the figure legends. The publisher regrets the error. The corrected figure legends are as follows:
Figure 1. A, Messenger (mRNA) expression of phosphatidylinositol-3-kinase catalytic subunit (PI3K in endothelial progenitor cells [EPCs], CD34+ cells, human umbilical vein endothelial cells (HUVECs), and CD14+ monocytes were assessed by microarray (n=3 to 4 each). The data are presented as mean±SEM. B, Protein expression of PI3K was assessed in EPCs from 5 different donors by Western blot. C, mRNA expression of PI3K in migrated vs nonmigrated EPCs was assessed by microarray (n=4 each). The data are presented as mean±SEM.
Figure 2. Role of PI3K for the matrix migration of human EPCs and murine BM Lin– progenitor cells. A through C, EPC migration on fibronectin was performed. EPCs were preincubated with the indicated inhibitors or dimethyl sulfoxide (DMSO). EPC migration was stimulated with the addition of phosphate-buffered saline (PBS; control), stromal cell–derived factor (SDF)1
(A and B), or interleukin (IL)-8 (C) in the lower chambers. Data are presented as the percentage of cells that migrated in comparison with nonstimulated control (which was set as 100% ±SEM) (A, *P<0.05 vs SDF1+DMSO, n=3 to 7; B, *P<0.05 vs SDF1+DMSO, n=7 to 9; C, *P<0.05 vs IL-8+DMSO, n=4). D, The migration of BM Lin– progenitor cells derived from wild-type (WT) and PI3K-deficient mice on fibronectin was stimulated with SDF1 or PBS (control). Data are presented as the percentage of cells that migrated to the lower chamber of the Transwell among the total cells put in the upper chamber of the Transwell (input) ±SEM. *P<0.05 vs WT+SDF1; 
P<0.05 vs WT+control; #P<0.05 vs PI3K-deficient+control (n=3). Abbreviations as in Figure 1.
Figure 3. Role of PI3K for the transendothelial migration (diapedesis) of progenitor cells. EPCs were preincubated where indicated with DMSO or the indicated inhibitors diluted in DMSO (LY294002 10 µmol/L or AS605240 200 nmol/L). After removal of the inhibitors and DMSO, the transendothelial migration of EPCs was stimulated where indicated with SDF1 for 18 hours. Data are presented as the percentage of cells that transmigrated in comparison with nonstimulated control (which was set as 100%) ±SEM. *P<0.05 vs SDF1+DMSO (n=9 to 10). Abbreviations as in Figures 1 and 2.
Figure 4. Role of PI3K for the adhesion of progenitor cells. A, SDF1 was immobilized where indicated on HUVEC monolayers. EPCs were preincubated with DMSO or the indicated inhibitors. After removal of DMSO and the inhibitors, EPCs were added to the HUVEC monolayers. The data are presented as mean±SEM (n=5 to 6; *P<0.05 vs SDF1+DMSO). B, SDF1 was immobilized where indicated on intercellular adhesion molecule (ICAM)-1–coated wells. EPCs were preincubated with DMSO or the indicated inhibitors. Adhesion of EPCs to ICAM-1–coated plates was detected after 10 minutes. The data are presented as mean±SEM (n=5; *P<0.05 vs SDF1+DMSO). C, EPCs (preincubated with DMSO or AS605240) were allowed to come in contact with a flow chamber slide coated with ICAM-1 or ICAM-1 and SDF1. Increasing levels of shear stress were applied to EPCs, and the adhering EPCs were assessed. The resistance of EPCs to detachment on increasing levels of shear stress as a direct measure of the adhesion function was evaluated. The data are presented as mean±SD (n=3; *P<0.05 vs SDF1+DMSO; #P<0.05 vs control+DMSO). D, Murine SDF1 was immobilized where indicated on ICAM-1–coated wells. BM Lin– progenitor cells derived from WT or PI3K-deficient mice on fibronectin were added to the ICAM-1–coated wells. Adhesion of Lin– cells was detected after 15 minutes. Data are presented as the percentage of the adhering cells among the total cells put in the well (input) ±SEM. *P<0.05 vs WT+SDF1 (n=4). Abbreviations as in Figures 1 and 2.
Figure 5. Role of PI3K for the affinity regulation of integrins in progenitor cells. A and B, For detection of activation-dependent epitopes on β2 integrins, EPCs were incubated with CBRM1/5 (A) or mAb24 (B) or the respective isotope control antibodies in the presence of SDF1 (200 ng/mL) or PBS (control). EPCs were preincubated where indicated with the respective inhibitors. The data are presented as mean±SEM (A, n=7, *P<0.05 vs SDF1+DMSO; B, n=14, *P<0.05 vs SDF1+DMSO). C, Binding of soluble vascular cell adhesion molecule (VCAM)-1/Fc was assessed in WT and PI3K-deficient BM cells in the presence of SDF1 (800 ng/mL), PBS (control), or MnCl2 (1 mmol/L). The data are presented as mean±SEM. #P<0.05 vs WT+control; *P<0.05 vs WT+SDF1 (n=11 to 14). n.s. indicates not significant. Abbreviations as in Figures 1 and 2.
Figure 6. Role of PI3K for in vivo homing an neovascularization-promoting capacity of progenitor cells. A, Cell Tracker Red–labeled BM Lin– progenitor cells from WT or PI3K-deficient mice were intravenously injected in nude mice 1 day after the induction of hindlimb ischemia. After 24 hours, the ischemic muscles were harvested and the number of progenitor cells was assessed in the ischemic muscles by microscopy (*P<0.05 vs WT cells, n=4 in each group; the data are presented as mean±SEM). B, BM Lin– progenitor cells from WT or PI3K-deficient mice or PBS (control, no cells) were intravenously injected in nude mice 1 day after the induction of hindlimb ischemia. After 15 days, the ischemic muscles were harvested and the capillary density was assessed by microscopy as described in Materials and Methods. The data are presented as mean±SD. *P<0.05 vs WT cells; #P<0.05 vs PBS (no cells; n=3 to 4). Abbreviations as in Figures 1 and 2.
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