Exogenous nitric oxide stimulated collagen type I expression and TGF-beta1 production in keloid fibroblasts by a cGMP-dependent manner

English | 正體中文 | 简体中文 | 全文笔数/总笔数 : 45346/58522 (77%)
造访人次 : 2503750 在线人数 : 195

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

Taipei Medical University Institutional Repository > 醫學院 > 臨床醫學研究所 > 期刊論文 > Item 987654321/3114

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://libir.tmu.edu.tw/handle/987654321/3114

题名:	Exogenous nitric oxide stimulated collagen type I expression and TGF-beta1 production in keloid fibroblasts by a cGMP-dependent manner
作者:	李婉若 Hsu YC;Hsiao M;Chien YW;Lee WR
贡献者:	臨床醫學研究所
日期:	2007
上传时间:	2009-08-21 16:58:29 (UTC+8)
摘要:	Keloids arise from the aberrant wound healing process and nitric oxide (NO) plays an important role in the inflammation stage of wound healing. In order to better define the potential effect of NO/cGMP signal pathway in the keloid pathogenesis, the enhancing effect of exogenous NO (released from NO donor) on collagen expression in the keloid fibroblast (KF) as well as on the induction of collagen type I protein and TGF-beta1 expression in the KF were studied in this investigation. The DETA NONOate, an NO donor, was added to the KF, as the exogenous NO, to release NO in the culture medium. The expression of collagens was then determined by assaying the total soluble collagens and collagen type I in the KF. The cellular concentration of cGMP was measured by EIA in the KF. Exogenous NO was found to enhance the expression of collagens and elevate the cellular levels of cGMP. Moreover, to evaluate the effect of the elevated cellular cGMP levels on the expression of collagen and TGF-beta1, both cGMP and TGF-beta1 were measured by ELISA. The inhibitors for phosphodiesterase (PDE), such as IBMX (3-isobutyl-1-methylxanthine), Vinpocetine, EHNA, Milrinone and Zapriast, which have been reported to reduce the ability of PDE and subsequently produce an increase of cellular cGMP, induce the production of autocrine TGF-beta1 as well as the synthesis of collagen in the KF. In this investigation, the inhibition of the PDE enzyme activity was observed to enhance the effect on the collagen synthesis, and was induced by exogenous NO. Taken together, these results have suggested that the NO/cGMP pathway could positively influence the progression of keloid formation, via the TGF-beta1 expression in the KF.
關聯:	Nitric oxide.(16):258-265.
数据类型:	article
显示于类别:	[臨床醫學研究所] 期刊論文

文件中的档案:

档案	大小	格式	浏览次数
全文.txt	0Kb	Text	285	检视/开启
摘要	34Kb	Adobe PDF	56	检视/开启
摘要.pdf	136Kb	Adobe PDF	45	检视/开启

在TMUIR中所有的数据项都受到原著作权保护.

TAIR相关文章

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.

数据加载中.....