Kwon H M, Itoh T, Rim J S, Handler J S
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Biochem Biophys Res Commun. 1995 Aug 24;213(3):975-9. doi: 10.1006/bbrc.1995.2224.
Kidney derived MDCK cells are protected from the stress of hypertonicity by accumulating compatible osmolytes. Accumulation of the compatible osmolytes myo-inositol and betaine is driven by hypertonicity-induced stimulation of transcription of the genes coding for the myo-inositol cotransporter and the betaine cotransporter. We tested the importance of the mitogen-activated protein kinase pathway in transcriptional activation of the genes for the two osmolytes cotransporters because this kinase pathway is rapidly activated when cells are exposed to hypertonicity and a mitogen-activated protein kinase pathway is essential for the osmo-protective transcriptional response of yeast to hypertonicity. Eliminating the activation of mitogen-activated protein kinase did not block the hypertonicity induced increase in accumulation of osmolyte transporter mRNA.
肾源性MDCK细胞通过积累相容性渗透剂来抵御高渗应激。相容性渗透剂肌醇和甜菜碱的积累是由高渗诱导的编码肌醇共转运蛋白和甜菜碱共转运蛋白的基因转录刺激所驱动的。我们测试了丝裂原活化蛋白激酶途径在两种渗透剂共转运蛋白基因转录激活中的重要性,因为当细胞暴露于高渗环境时,该激酶途径会迅速被激活,并且丝裂原活化蛋白激酶途径对于酵母对高渗的渗透保护转录反应至关重要。消除丝裂原活化蛋白激酶的激活并没有阻止高渗诱导的渗透剂转运蛋白mRNA积累的增加。