Suppression of type I collagen production by microRNA-29b in cultured human stellate cells

被引：111

作者：

Ogawa, Tomohiro

Iizuka, Masashi

Sekiya, Yumiko ^{[2
]}

Yoshizato, Katsutoshi ^{[3
]}

Ikeda, Kazuo ^{[4
]}

Kawada, Norifumi ^{[1
]}

机构：

[1] Osaka City Univ, Grad Sch Med, Dept Hepatol, Abeno Ku, Osaka 5458585, Japan

[2] Toray Industries Ltd, Kanagawa, Japan

[3] PhoenixBio Co Ltd, Hiroshima, Japan

[4] Nagoya City Univ, Grad Sch Med, Dept Funct Anat, Aichi, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2010年 / 391卷 / 01期

关键词：

Liver fibrosis; SP1; TGF-beta; Interferon; TargetScan; HEPATIC-FIBROSIS; LIVER-CANCER; INTERFERON; EXPRESSION; TRANSCRIPTION; SP1; DIFFERENTIATION; MODULATION; MECHANISM; INJURY;

D O I：

10.1016/j.bbrc.2009.11.056

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

MicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression through imperfect base pairing with the 3' untranslated region (3'UTR) of target mRNA. We Studied the regulation of alpha 1 (1) collagen (Col1A1) expression by miRNAs in human stellate cells. which are involved in liver fibrogenesis. Among miR-29b, -143, and -218, whose expressions were altered in response to transforming growth factor-beta 1 or interferon-alpha stimulation, miR-29b was the most effective Suppressor of type I collagen at the mRNA and protein level via its direct binding to Col1A1 3'UTR miR-29b also had an effect on SP1 expression These results suggested that miR-29b is involved in the regulation of type I collagen expression by interferon-alpha in hepatic stellate cells. It is anticipated that miR-29b will be used for the regulation of stellate cell activation and lead to antifibrotic therapy (C) 2009 Elsevier Inc All rights reserved.

引用

页码：316 / 321

页数：6

共 31 条

[1]

Albanis E, 2001, Clin Liver Dis, V5, P315, DOI 10.1016/S1089-3261(05)70168-9

[2]

ALBANIS E, 2001, CLIN LIVER DIS, V5, pR5

[3] MicroRNAs: Genomics, biogenesis, mechanism, and function (Reprinted from Cell, vol 116, pg 281-297, 2004) [J].