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-actin filaments in venous smooth muscle
cells in response to mechanical stretch
Biomedical Engineering Department, Northwestern University, Evanston, Illinois 60208-3107
Mechanical stretch has been shown
to induce the degradation of 
-actin filaments in smooth muscle cells
(SMC) of experimental vein grafts. Here, we investigate the possible
role of ERK1/2 and p38 MAPK in regulating this process 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 was reduced significantly under arterial
pressure (91 ± 1%, 43 ± 13%, 51 ± 5%, 28 ± 3%, and 19 ± 5% at 1, 6, 12, 24, and 48 h, respectively),
whereas 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 h, respectively) and a decrease in SMC density (from
the control level of 1,368 ± 66 cells/mm2 at
time 0 to 1,205 ± 90, 783 ± 129, 845 ± 61, 637 ± 55, and 432 ± 125 cells/mm2 at 1, 6, 12 , 24, and 48 h of exposure to arterial pressure, respectively).
Treatment with a p38 MAPK inhibitor (SB-203580) significantly reduced
the stretch-induced activation of caspase 3 at 6 h (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. Treatment with an inhibitor for the
ERK1/2 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.
mitogen-activated protein kinases; caspase 3; vascular grafts
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