Retinoic acid inhibits inducible nitric oxide synthase expression in 3T3-L1 adipocytes

The present study was undertaken to explore whether retinoids, which are known to have immunomodulatory actions, could attenuate tumor necrosis factor-alpha (TNF)-stimulated inducible nitric oxide synthase (iNOS) expression in 3T3-L1 adipocytes. Adipocytes incubated with TNF induced dose- and time-d...

Full description

Saved in:
Bibliographic Details
Published in:Experimental & molecular medicine 2002-11, Vol.34 (5), p.353-360
Main Authors: Yang, Jeong-Yeh, Koo, Bon-Sun, Kang, Mi-Kyung, Rho, Hye-Won, Sohn, Hee-Sook, Jhee, Eun-Chung, Park, Jin-Woo
Format: Article
Language:English
Subjects:
3T3 Cells
Adipocytes - drug effects
Adipocytes - enzymology
Adipocytes - metabolism
Animals
Cells, Cultured
Enzyme Induction - drug effects
Enzyme Inhibitors - pharmacology
Lipoprotein Lipase - drug effects
Lipoprotein Lipase - metabolism
Mice
NF-kappa B - antagonists & inhibitors
Nitric Oxide - metabolism
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase - metabolism
Nitric Oxide Synthase Type II
Tretinoin - pharmacology
Tumor Necrosis Factor-alpha - pharmacology
Citations: Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The present study was undertaken to explore whether retinoids, which are known to have immunomodulatory actions, could attenuate tumor necrosis factor-alpha (TNF)-stimulated inducible nitric oxide synthase (iNOS) expression in 3T3-L1 adipocytes. Adipocytes incubated with TNF induced dose- and time-dependent accumulation of nitrite in the culture medium through the iNOS induction as confirmed by Western blotting. Treatment of cells with TNF in the presence of all-trans-retinoic acid (RA) significantly decreased their ability to produce nitrite and iNOS induction. Both 13-cis- and all- trans-RA-induced suppression was dose-dependent, and all-trans-RA was somewhat potent than 13-cis-RA. The inhibitory effect of RA on TNF-induced iNOS induction was reversible, completely recovered after 2 days, and was exerted through the inhibition of NF-kappaB activation. TNF also suppressed the lipoprotein lipase (LPL) activity of 3T3-L1 adipocytes. RA could not reverse the TNF- induced LPL suppression at RA levels causing near complete inhibition of the TNF-induced NO production. These results indicate that RAs attenuate iNOS expression reversibly in TNF-stimulated 3T3-L1 adipocytes, and that the TNF-induced LPL suppression is not the result of NO overproduction.
ISSN:1226-3613
2092-6413
2092-6413
DOI:10.1038/emm.2002.50