The antifibrotic effect of TGF-beta1 siRNAs in murine model of liver cirrhosis.

Full Abstract

Liver fibrosis results from chronic damage to the liver by chronic hepatitis, alcohol, and toxic agents. A characteristic of liver fibrosis is an accumulation of extracellular matrix (ECM) protein, which distorts the hepatic architecture by forming a fibrous scar, and the subsequent development of regenerating nodules defines cirrhosis. Transforming growth factor (TGF)-beta1, one of the most powerful profibrogenic mediators, plays a major role in the development of liver cirrhosis and regulates ECM gene expression and matrix degradation. This study elucidates the changes of TGF-beta1-mediated signals during liver fibrogenesis by using RNA interference. In this experiment, the TGF-beta1 siRNAs reduced the expression of TGF-beta1 in the livers of CCl(4) injection compared with those of control group, and the expression of type I collagen and alpha-smooth muscle actin was decreased. In conclusion, this study demonstrates that TGF-beta1 siRNAs inhibit TGF-beta1 expression in the murine model of liver cirrhosis and might be a good therapeutic strategy to prevent liver cirrhosis in human.

Author information

Author/s: Kim, Kyung-Hyun (KH); Kim, Hyun-Chul (HC); Hwang, Mee-Yul (MY); Oh, Hoon-Kyu (HK); Lee, Tae-Sung (TS); Chang, Young-Chae (YC); Song, Ho-Jung (HJ); Won, Nam-Hee (NH); Park, Kwan-Kyu (KK);

Affiliation: Department of Pathology, Catholic University of Daegu, College of Medicine, 3056-6 Daemyung 4-Dong, Nam-Gu, Daegu 705-718, Republic of Korea.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun), published in United States. (Language: eng)

Reference: 2006-May; vol 343 (issue 4) : pp 1072-8

Dates: Created 2006/04/26; Completed 2006/06/09; Revised 2006/11/15;

PMID: 16579972, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Actins - metabolism
Animals
Carbon Tetrachloride Poisoning - metabolism; pathology
Collagen Type I - metabolism
Extracellular Matrix - metabolism
Liver - metabolism; pathology
Liver Cirrhosis, Experimental - chemically induced; metabolism; pathology

Liver Cirrhosis, Experimental - chemically induced; metabolism; pathology
Mice
Mice, Inbred C57BL
RNA Interference
RNA, Small Interfering - physiology
Transforming Growth Factor beta - biosynthesis; genetics
Transforming Growth Factor beta1

Associated Chemicals: Actins (0) ; Collagen Type I (0) ; RNA, Small Interfering (0) ; TGFB1 protein, human (0) ; Tgfb1 protein, mouse (0) ; Transforming Growth Factor beta (0) ; Transforming Growth Factor beta1 (0)

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