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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Sotoda Y,Negoro M,Wakabayashi Idoi
10.1016/s0014-5793(02)02747-3keywords:
subject
Has Abstractpub_date
2002-05-22 00:00:00pages
227-30issue
1-3eissn
0014-5793issn
1873-3468pii
S0014579302027473journal_volume
519pub_type
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