- 作者: Sammy Saab a, Steven P. Tam a, Binh N. Tran a, Andrew C. Melton b, Pisit Tangkiivanich a, Helen Wong a,c, Hal F. Yee, Jr. a-c
- 作者服務機構: Departments of a Medicine and b Physiology, and c CURE Digestive Diseases Research Center, UCLA School of Medicine, Los Angeles, Calif, USA
- 中文摘要: --
- 英文摘要: generation. Y-27632, which selectively inhibits rho-asso-ciated kinase, also blocked endothelin-1-stimulated myo-sin phosphorylation and contractile force generationwith a similar dose dependence. These results suggestthat endothelin-1-stimulated contractile force generationby stellate cells is mediated by myosin.Although endothelin-1-stimulated contractile force gen-eration by stellate cells is believed to play an importantrole in hepatic pathophysiology, the molecular signalsthat mediate this process are incompletely understood.The aim of this study was to test the hypothesis thatmyosin mediates the contractile force generated by stel-late cells in response to endothelin-1. Contractile forcegeneration by primary and immortalized stellate cellswas directly and quantitatively measured. Myosin phos-phorylation and reorganization, and actin stressfiberfor-mation were investigated in immortalized stellate cells.Endothelin-1 stimulated a rapid and robust generation ofcontractile force by primary and immortalized stellatecells with a similar dose dependence. Myosin phosphor-ylation, actin stress fiber assembly, and reorganization ofmyosin to stress fibers were induced by concentrationsof endothelin-1 that also stimulated stellate cell contrac-tion. BQ-123, a selective endothelin receptor antagonist,inhibited myosin phosphorylation and contractile force
- 中文關鍵字: --
- 英文關鍵字: Actin, Myosin regulatory light chain, Phosphorylation, Signal transduction