The essential role of Oct-2 in LPS-induced expression of iNOS in Raw 264.7 macrophages and its regulation by Trichostatin A

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Title:	The essential role of Oct-2 in LPS-induced expression of iNOS in Raw 264.7 macrophages and its regulation by Trichostatin A
Authors:	張淑芬 Shao-chun Lu;Hsiao-Wen Wu;Yen-Jen Lin;Shwu-Fen Chang
Contributors:	醫學科學研究所
Date:	2009
Issue Date:	2009-08-25 09:56:41 (UTC+8)
Abstract:	This article reports on a study of the effect of trichostatin A (TSA), an inhibitor of histone deacetylase, on lipopolysaccharide (LPS)-induced expression of inducible nitric oxide synthase (iNOS) in RAW 264.7 macrophages and its underlying mechanisms. TSA pretreatment potently diminishes LPS-stimulated nitric oxide (NO) release and both mRNA and protein levels of iNOS in macrophages. The effects of TSA and LPS on transcription factors binding to two LPS-responsive elements within the iNOS promoter, one binding the NF-kappaB site and the other the octamer element, were investigated. Results show that TSA did not alter the LPS-activated NF-kappaB activity demonstrated by the nuclear translocation of p50 and p65 and by a NF-kappaB-driven reporter gene expression system. In addition, neither TSA nor LPS changed the expression of Oct-1, a ubiquitously expressed octamer binding protein. However, TSA suppressed the LPS-induced expression of Oct-2, another octamer binding protein, at both mRNA and protein levels. Chromatin immunoprecipitation assays revealed that binding of Oct-2 to the iNOS promoter was enhanced by LPS treatment; however, pretreatment with TSA resulted in loss of this binding. Moreover, forced expression of Oct-2 by transfection of pCG-Oct-2 plasmid restored the TSA-suppressed iNOS expression elevated by LPS stimulation, further indicating that Oct-2 activation is a crucial step for transcriptional activation of the iNOS gene in response to LPS stimulation in macrophages. This study demonstrates that TSA diminishes iNOS expression in LPS-treated macrophages by inhibiting Oct-2 expression and thus reducing the production of NO.
Relation:	American Journal of Physiology - Cell Physiology.(296):1133-1139.
Data Type:	article
Appears in Collections:	[Graduate Institute of Medical Sciences] Periodical Article

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