转化生长因子-β介导的肾小管上皮细胞增殖涉及百日咳毒素敏感的G蛋白和蛋白激酶C依赖性途径。

Transforming growth factor-beta-mediated proliferation of renal tubular epithelial cells involves pertussis toxin-sensitive G protein-and protein kinase C-dependent pathways.

作者信息

Wu H L, Nambi P

机构信息

Department of Renal Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, PA 19406-0939, USA.

出版信息

Pharmacology. 1998 Jul;57(1):8-12. doi: 10.1159/000028220.

DOI:10.1159/000028220

PMID:9670207

Abstract

Exposure of LLCPK-1 cells to transforming growth factor (TGF)-beta(1) resulted in an increase in [3H]thymidine incorporation. This increase depended on the concentration of TGF-beta(1) used with an EC50 value of 0.3-1 pmol/l. Concentrations > 10 pmol/l were inhibitory. Similar effects occurred with TGF-beta(3). Addition of both TGF-beta(1) and TGF-beta(3) together had no additive effect. Pretreatment of cells with 10 mumol/1 genestein exerted no effect on TGF-beta-mediated response, whereas pretreatment with 10 mumol/1 Ro-32-0432 inhibited TGF-beta-mediated [3H]thymidine incorporation. In addition, pretreatment of cells with pertussis toxin attenuated TGF-beta-mediated proliferation of LLCPK-1 cells. These data indicate that in LLCPK-1 cells, TGF-beta(1) and TGF-beta(3) mediate their responses through the same receptor. This pathway involves protein kinase C and pertussis toxin-sensitive G protein.

摘要

将LLCPK - 1细胞暴露于转化生长因子（TGF）-β(1)会导致[3H]胸苷掺入增加。这种增加取决于所使用的TGF-β(1)的浓度，其半数有效浓度（EC50）值为0.3 - 1皮摩尔/升。浓度大于10皮摩尔/升则具有抑制作用。TGF-β(3)也有类似作用。同时添加TGF-β(1)和TGF-β(3)没有相加效应。用10微摩尔/升染料木黄酮预处理细胞对TGF-β介导的反应没有影响，而用10微摩尔/升Ro - 32 - 0432预处理则抑制TGF-β介导的[3H]胸苷掺入。此外，用百日咳毒素预处理细胞会减弱TGF-β介导的LLCPK - 1细胞增殖。这些数据表明，在LLCPK - 1细胞中，TGF-β(1)和TGF-β(3)通过相同的受体介导其反应。该途径涉及蛋白激酶C和对百日咳毒素敏感的G蛋白。