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首页> 外文期刊>Journal of Cellular Physiology >p38 MAP kinase mediates platelet-derived growth factor-stimulated migration of hepatic myofibroblasts.
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p38 MAP kinase mediates platelet-derived growth factor-stimulated migration of hepatic myofibroblasts.

机译：p38 MAP激酶介导的血小板源生长factor-stimulated迁移肝myofibroblasts。

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摘要

Although the migration of hepatic myofibroblasts (HMFs) contributes to the development of fibrosis, the signals regulating migration of these cells are poorly understood. In this study, we tested the hypothesis that HMF migration is stimulated by platelet-derived growth factor-BB (PDGF-BB) through p38 mitogen-activated protein (MAP) kinase and extracellular signal-regulated kinase (ERK) signaling pathways. This hypothesis was addressed by directly visualizing the migration of cultured human HMFs into a wound. PDGF-BB stimulated membrane ruffling, migration, and proliferation. PDGF-BB also induced activation of p38 MAP kinase, its downstream effector, heat shock protein (HSP) 27, ERK 1 and ERK 2, and p125 focal adhesion kinase (FAK). Selective antagonism of p38 MAP kinase blocked PDGF-BB-stimulated HSP 27 phosphorylation, membrane ruffling, and migration, but did not alter PDGF-BB-induced proliferation. Selective antagonism of ERK kinase inhibited PDGF-BB-induced ERK phosphorylation and proliferation, but did not affect PDGF-BB-stimulated migration. Concentrations of PDGF-BB that stimulated migration and proliferation did not influence myosin-dependent contractility. Neither selective inhibition of p38 MAP kinase nor ERKs altered PDGF-BB-induced activation of FAK. In conclusion, these results provide novel evidence indicating that (1) HMF migration is stimulated by PDGF-BB through the regulation of membrane ruffling by a p38 MAP kinase signaling pathway, (2) whereas p38 MAP kinase mediates PDGF-BB-stimulated migration, but not proliferation, ERKs mediate PDGF-induced proliferation, but not migration, and (3) increases in myosin-dependent contractility are not required for PDGF-BB-stimulated migration.
机译：尽管肝myofibroblasts的迁移(羟甲基糠醛)导致的发展纤维化的信号调节的迁移这些细胞是知之甚少。我们测试了羟甲基糠醛迁移的假设通过血小板源生长factor-BB刺激通过p38增殖作用(PDGF-BB)(地图)激酶和细胞外signal-regulated激酶(ERK)信号通路。解决了直接可视化人工培养的羟甲基糠醛的迁移到伤口。PDGF-BB刺激膜激怒,迁移,和扩散。p38 MAP激酶激活,其下游效应,热休克蛋白(HSP) 27日,ERK 1和ERK 2, p125粘着斑激酶(FAK)。选择性p38 MAP激酶拮抗阻塞PDGF-BB-stimulated HSP 27磷酸化,膜波动,和迁移,但没有改变PDGF-BB-induced扩散。ERK激酶抑制拮抗作用PDGF-BB-induced ERK的磷酸化和扩散,但并不影响PDGF-BB-stimulated迁移。PDGF-BB迁移和刺激myosin-dependent扩散并没有影响收缩性。p38 MAP激酶erk PDGF-BB-induced改变FAK的激活。提供新的证据表明(1)羟甲基糠醛迁移是由PDGF-BB通过刺激调节膜激怒p38地图激酶信号通路,(2)而p38地图激酶介导PDGF-BB-stimulated迁移,但是不扩散,erk PDGF-induced调停扩散,但不是移民,和(3)增加myosin-dependent收缩性不需要PDGF-BB-stimulated迁移。

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