肌醇转运减少参与脂多糖诱导的血管平滑肌磷酸肌醇水解抑制。

Involvement of decreased myo-inositol transport in lipopolysaccharide-induced depression of phosphoinositide hydrolysis in vascular smooth muscle.

作者信息

Sotoda Yoko, Negoro Munetaka, Wakabayashi Ichiro

机构信息

Department of Hygiene and Preventive Medicine, School of Medicine, Yamagata University, Iida-Nishi 2-2-2, Yamagata, Japan.

出版信息

FEBS Lett. 2002 May 22;519(1-3):227-30. doi: 10.1016/s0014-5793(02)02747-3.

DOI:10.1016/s0014-5793(02)02747-3

PMID:12023050

Abstract

The mechanism underlying lipopolysaccharide (LPS)-induced depression of phosphoinositide (PI) hydrolysis was investigated using rat aortas. In LPS-pretreated aortas, the 5-hydroxytryptamine-stimulated accumulation of inositol monophosphate and incorporation of exogenous myo-inositol into PIs were significantly less than those in control aortas. Both sodium-myo-inositol cotransporter (SMIT) and phosphatidylinositol transfer protein (PITP) genes were constituently expressed in rat aortas. The mRNA level of SMIT was remarkably lower in LPS-pretreated aortas, while that of PITP mRNA was not affected by LPS. These results suggest that LPS-induced depression of SMIT expression is involved in inhibition of agonist-stimulated PI hydrolysis by LPS.

摘要

利用大鼠主动脉研究了脂多糖（LPS）诱导磷酸肌醇（PI）水解降低的机制。在经LPS预处理的主动脉中，5-羟色胺刺激的肌醇单磷酸积累以及外源性肌醇掺入PI中的量均显著低于对照主动脉。钠-肌醇共转运体（SMIT）和磷脂酰肌醇转移蛋白（PITP）基因在大鼠主动脉中均持续表达。经LPS预处理的主动脉中SMIT的mRNA水平显著降低，而PITP mRNA水平不受LPS影响。这些结果表明，LPS诱导的SMIT表达降低与LPS抑制激动剂刺激的PI水解有关。