Premium
Involvement of decreased myo‐inositol transport in lipopolysaccharide‐induced depression of phosphoinositide hydrolysis in vascular smooth muscle
Author(s) -
Sotoda Yoko,
Negoro Munetaka,
Wakabayashi Ichiro
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)02747-3
Subject(s) - inositol , phosphatidylinositol , lipopolysaccharide , chemistry , medicine , endocrinology , inositol phosphate , hydrolysis , intracellular , vascular smooth muscle , biochemistry , receptor , signal transduction , biology , smooth muscle
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.