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1 Department of Bioengineering and Whitaker Institute of Biomedical Engineering, 2 Advanced Tissue Sciences, La Jolla 92037; 3 Division of Biomedical Sciences, University of California, Riverside 92506; and 4 Department of Medicine, University of California, San Diego, La Jolla, California 92093
We
studied the response of porcine vascular smooth muscle cells
(PVSMCs) to cyclic sinusoidal stretch at a frequency of 1 Hz. Cyclic
stretch with an area change of 25% caused an increase in PVSMC
apoptosis, which was accompanied by sustained activation of
c-Jun NH2-terminal kinases (JNK) and the mitogen-activated protein kinase p38. Cyclic stretch with an area change of 7% had no
such effect. Infection of PVSMCs with recombinant adenoviruses expressing constitutively active forms of upstream molecules that activate JNK and p38 also led to apoptosis. The simultaneous
blockade of both JNK and p38 pathways with adenovirus-mediated
expression of dominant-negative mutants of c-Jun and p38 caused a
significant decrease (to 1/2) of the apoptosis induced by 25%
cyclic stretch. The 25% stretch also caused sustained clustering of
tumor necrosis factor-
(TNF-) receptor-1 and its association with
TNF- receptor-associated factor-2 (TRAF-2). Overexpressing the
wild-type TRAF-2 in PVSMCs caused an increase in apoptosis. In
contrast, the expression of a dominant-negative mutant of TRAF-2
attenuated stretch-induced apoptois. These results support the
hypothesis that circumferential overload under hypertensive conditions
induces a clustering of death receptors that cause vascular smooth
muscle cell apoptosis.
c-Jun NH2-terminal kinases; p38; mechanotransduction; mechanical overload; vascular wall
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