Marunaka Y, Shintani Y, Sugimoto E, Niisato N
MRC Group in Lung Development, Hospital for Sick Children Research Institute, University of Toronto, Faculty of Medicine, Toronto, Ontario, Canada M5G 1X8.
Pflugers Arch. 1996 Jul;432(3):571-3. doi: 10.1007/s004240050171.
The aim of the present study was to investigate the roles of tyrosine kinase (TK) in the insulin action on cell volume in fetal rat (20-day gestational age) type II pneumocyte. Insulin (100 nmol/l) increased cell volume, and this insulin (100 nmol/l) action was completely blocked by 50 micromol/l bumetanide (BMT) and 10 micromol/l amiloride (AML). This observation indicates that 100 nmol/l insulin activates BMT-sensitive Na+/K+/2Cl- cotransporter and AML-sensitive pathways. The stimulatory action of 100 nmol/l insulin on BMT-sensitive Na+/K+/2Cl- cotransporter was completely abolished by 10 micromol/l lavendustin A (LAV-A, an inhibitor of TK), however 100 nmol/l insulin could stimulate AML-sensitive pathways even in LAV-A (10 micromol/l)-treated cells. These observations indicate that the insulin (100 nmol/l) action on the BMT-sensitive Na+/K+/2Cl- cotransporter is mediated through TK-dependent pathways, while 100 nmol/l insulin requires a TK-independent pathway to show the stimulatory action on the AML-sensitive pathways. From these observations we conclude that TK-dependent and -independent pathways are involved in the insulin (100 nmol/l) signaling in fetal rat type II pneumocyte.
本研究的目的是探讨酪氨酸激酶（TK）在胰岛素对胎鼠（妊娠20天）II型肺细胞体积作用中的角色。胰岛素（100 nmol/l）可增加细胞体积，而这种胰岛素（100 nmol/l）的作用被50 μmol/l布美他尼（BMT）和10 μmol/l阿米洛利（AML）完全阻断。该观察结果表明，100 nmol/l胰岛素激活了BMT敏感的Na+/K+/2Cl-共转运体和AML敏感途径。10 μmol/l拉文达斯汀A（LAV-A，一种TK抑制剂）可完全消除100 nmol/l胰岛素对BMT敏感的Na+/K+/2Cl-共转运体的刺激作用，然而，即使在经LAV-A（10 μmol/l）处理的细胞中，100 nmol/l胰岛素仍可刺激AML敏感途径。这些观察结果表明，胰岛素（100 nmol/l）对BMT敏感的Na+/K+/2Cl-共转运体的作用是通过TK依赖性途径介导的，而100 nmol/l胰岛素需要一条不依赖TK的途径来显示其对AML敏感途径的刺激作用。从这些观察结果我们得出结论，TK依赖性和非依赖性途径参与了胎鼠II型肺细胞中胰岛素（100 nmol/l）的信号传导。
