Ikejima K, Watanabe S, Kitamura T, Hirose M, Miyazaki A, Sato N
Department of Gastroenterology, Juntendo University School of Medicine, Tokyo, Japan.
Biochem Biophys Res Commun. 1995 Sep 14;214(2):440-6. doi: 10.1006/bbrc.1995.2306.
We demonstrated that HGF reduces gap junctional intercellular communication of rat hepatocyte doublets and increases cell spreading. Intercellular communication via gap junctions was markedly reduced in hepatocyte doublets with HGF (20 ng/ml) 3-12 hr after inoculation. Immunocytochemistry revealed spotty localization of connexin 32 on the plasma membrane of 3-hr cultured control hepatocyte doublets, whereas HGF-treated doublets showed significantly less connexin 32 staining. Genistein maintained intercellular communication in the presence of HGF, indicating that HGF reduces intercellular communication by down regulation of connexin 32 through the c-met/HGF receptor-tyrosine-kinase-mediated pathway. Furthermore, TGF-beta 1 maintained intercellular communication in the presence of HGF. Regulation of intercellular communication in hepatocytes by HGF and TGF-beta 1 might play an important role during liver regeneration.
我们证明，肝细胞生长因子（HGF）可减少大鼠肝细胞双联体的间隙连接细胞间通讯，并增加细胞铺展。接种后3 - 12小时，在含有HGF（20 ng/ml）的肝细胞双联体中，通过间隙连接的细胞间通讯显著减少。免疫细胞化学显示，在培养3小时的对照肝细胞双联体的质膜上，连接蛋白32呈斑点状定位，而经HGF处理的双联体显示连接蛋白32染色明显减少。金雀异黄素在有HGF存在的情况下维持细胞间通讯，表明HGF通过c-met/HGF受体酪氨酸激酶介导的途径下调连接蛋白32，从而减少细胞间通讯。此外，转化生长因子β1（TGF-β1）在有HGF存在的情况下维持细胞间通讯。HGF和TGF-β1对肝细胞间通讯的调节可能在肝脏再生过程中起重要作用。
