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

English | 正體中文 | 简体中文 | 全文筆數/總筆數 : 45346/58522 (77%)
造訪人次 : 2503621 線上人數 : 207

RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.

Taipei Medical University Institutional Repository > 醫學院 > 醫學科學研究所 > 期刊論文 > Item 987654321/3714

請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/3714

題名:	The essential role of Oct-2 in LPS-induced expression of iNOS in Raw 264.7 macrophages and its regulation by Trichostatin A
作者:	張淑芬 Shao-chun Lu;Hsiao-Wen Wu;Yen-Jen Lin;Shwu-Fen Chang
貢獻者:	醫學科學研究所
日期:	2009
上傳時間:	2009-08-25 09:56:41 (UTC+8)
摘要:	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.
關聯:	American Journal of Physiology - Cell Physiology.(296):1133-1139.
資料類型:	article
顯示於類別:	[醫學科學研究所] 期刊論文

文件中的檔案:

檔案	描述	大小	格式	瀏覽次數
233.pdf		477Kb	Adobe PDF	82	檢視/開啟
全文.txt		0Kb	Text	218	檢視/開啟

在TMUIR中所有的資料項目都受到原著作權保護.

TAIR相關文章

著作權聲明 Copyright Notice

本平台之數位內容為臺北醫學大學所收錄之機構典藏，包含體系內各式學術著作及學術產出。秉持開放取用的精神，提供使用者進行資料檢索、下載與取用，惟仍請適度、合理地於合法範圍內使用本平台之內容，以尊重著作權人之權益。商業上之利用，請先取得著作權人之授權。
The digital content on this platform is part of the Taipei Medical University Institutional Repository, featuring various academic works and outputs from the institution. It offers free access to academic research and public education for non-commercial use. Please use the content appropriately and within legal boundaries to respect copyright owners' rights. For commercial use, please obtain prior authorization from the copyright owner.
瀏覽或使用本平台，視同使用者已完全接受並瞭解聲明中所有規範、中華民國相關法規、一切國際網路規定及使用慣例，並不得為任何不法目的使用TMUIR。
By utilising the platform, users are deemed to have fully accepted and understood all the regulations set out in the statement, relevant laws of the Republic of China, all international internet regulations, and usage conventions. Furthermore, users must not use TMUIR for any illegal purposes.
本平台盡力防止侵害著作權人之權益。若發現本平台之數位內容有侵害著作權人權益情事者，煩請權利人通知本平台維護人員([email protected])，將立即採取移除該數位著作等補救措施。
TMUIR is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff([email protected]). We will remove the work from the repository.

資料載入中.....