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Actin Filaments in Venous Smooth Muscle Cells in Response to Mechanical Stretch
1 Biomedical Engineering, Northwestern University, Evanston, IL, USA
* To whom correspondence should be addressed. E-mail: jgo821{at}hecky.acns.nwu.edu.
Mechanical stretch has been shown to induce the degradation of 
-actin filaments in the smooth muscle cell (SMC) of experimental vein grafts. Here, we investigate the
possible role of extracellular signal-regulated kinase (ERK) 1/2 and p38 mitogenactivated protein kinase (MAPK) in regulating this process by using an ex vivo venous
culture model that simulates an experimental vein graft. An exposure of a vein to arterial pressure induced a significant increase in the medial circumferential strain, which induced rapid -actin filament disruption, followed by degradation. The percentage of SMC -actin filament coverage reduced significantly under arterial pressure (91+/-1%, 43+/-13%, 51+/-5%, 28+/-3%, and 19+/-5% at 1, 6, 12, 24, and 48 hrs, respectively), while it did not change significantly in specimens under venous pressure at theses times. The degradation of SMC -actin filaments paralleled an increase in the relative activity of caspase-3 (3.0+/-0.7 and 1.7+/-0.4 fold increase relative to the control level at 6 and 12 hrs, respectively) and a decrease in SMC density (from the control level 1368+/-66 cells/mm2 at time 0 to 1205+/-90, 783+/-129, 845+/-61, 637+/-55, and 432+/-125
cells/mm2 at 1, 6, 12 , 24, and 48 hrs of exposure to arterial pressure, respectively). A treatment with a p38 MAPK inhibitor (SB 203580) significantly reduced stretch-induced activation of caspase-3 at 6 hrs (from 3.0+/-0.7 to 2.2+/-0.3 fold), in conjunction with a significant rescue of -actin filament degradation (from 43+/-13% to 69+/-15%) at the same time. A treatment with an inhibitor for the ERK 1/2 activator (PD 98059), however, did not induce a significant change in the activity of caspase-3 or the percentage of SMC -actin filament coverage. These results suggest that p38 MAPK and caspase-3 may mediate stretch-dependent degradation of -actin filaments in vascular SMCs.
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