Activation of JNK/SAPK and ERK by mechanical strain in vascular smooth muscle cells depends on extracellular matrix composition

被引:88
作者
Reusch, HP
Chan, G
Ives, HE
Nemenoff, RA
机构
[1] UNIV CALIF SAN FRANCISCO, CARDIOVASC RES INST, SAN FRANCISCO, CA 94143 USA
[2] UNIV COLORADO, HLTH SCI CTR, DEPT MED, DIV RENAL DIS & HYPERTENS, DENVER, CO 80220 USA
关键词
D O I
10.1006/bbrc.1997.7121
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Application of cyclic mechanical strain to vascular smooth muscle (VSM) cells elicits distinct cellular responses depending on extracellular matrix composition. We now examine activation of p42/p44 MAP kinase (ERK) and c-jun amino terminal kinase (JNK/SAPK) by cyclic (1 Hz) mechanical strain in neonatal rat VSM cells cultured on pronectin or laminin. In cells grown on pronectin, mechanical strain activated both ERKs (peak 10-30 min) and JNK/SAPK (peak 15-30 min). On laminin, mechanical strain induced a comparable activation of JNK/SAPK to that seen on pronectin, but no significant activation of ERKs. In contrast, application of strain to adult VSM cells activated both enzymes independently of extracellular matrix composition. In neonatal VSM cells, cyclic strain induced SM-1 smooth muscle myosin in cells cultured on laminin, but not on pronectin, Thus in neonatal VSM cells, activation of ERKs and induction of SM-1 myosin by mechanical strain depend on extracellular matrix composition. (C) 1997 Academic Press.
引用
收藏
页码:239 / 244
页数:6
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