作者: Atsushi Masamune , Masahiro Satoh , Kazuhiro Kikuta , Noriaki Suzuki , Kennichi Satoh
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摘要: Aim Activated pancreatic stellate cells (PSCs) are implicated in the pathogenesis of fibrosis and inflammation. Endothelin-1 (ET-1), which acts through G-protein coupled ET(A) ET(B) receptors, has several biological activities. We here examined ability ET-1 to affect cell functions PSCs underlying molecular mechanisms. Methods were isolated from pancreas male Wistar rats after perfusion with collagenase, between passages two five used. Expression ET receptors was assessed by reverse transcription-PCR immunostaining. Phosphorylation myosin regulatory light chain (MLC), extracellular-signal regulated kinase (ERK), Akt Western blotting. Contraction on hydrated collagen lattices. Cell migration using modified Boyden chambers. proliferation measuring incorporation 5-bromo-2'-deoxyuridine. Results Culture-activated expressed ET-1. induced phosphorylation MLC ERK, but not Akt. contraction migration, did alter PSCs. ET-1-induced inhibited an receptor antagonist BQ-123 BQ-788, whereas BQ-788 BQ-123. A Rho inhibitor Y-27632 abolished both migration. Conclusion activation Rho-Rho kinase. play different roles regulation these cellular response