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

FEBS Letters

Wakabayashi, Ichiro¹  Sotoda, Yoko¹  Negoro, Munetaka¹ 

[1]Department of Hygiene and Preventive Medicine, School of Medicine, Yamagata University, Iida-Nishi 2-2-2, Yamagata 990-9585, Japan

关键词: Septic shock;    Phosphatidylinositols;    Inositol 1;    4;    5-trisphosphate;    Vasoconstriction;    Gene expression;    PI;    phosphoinositide;    LPS;    lipopolysaccharide;    SMIT;    sodium-myo-inositol cotransporter;    PITP;    phosphatidylinositol transfer protein;    NO;    nitric oxide;    5-HT;    5-hydroxytryptamine;    IP;    inositol monophosphate;    PLC;    phospholipase C;    DMEM;    Dulbecco's modified Eagle's medium;    CLP;    cecal ligation and puncture;    cDNA;    complementary DNA;    PCR;    polymerase chain reaction;    TNFα;    tumor necrosis factor-α;   

DOI  :  10.1016/S0014-5793(02)02747-3

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown