Liver Fibrosis Will Be Treated By A Potential Target

Main Category: Liver Disease / Hepatitis
Also Included In: Biology / Biochemistry
Article Date: 17 Oct 2007 - 7:00 PDT

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The outcome of hepatitis is either self recovery or its development into liver fibrosis or, further, liver cirrhosis. Liver fibrosis is the early pathological process of cirrhosis, which is considered a reversible, wound-healing response. Since no ideal drug is available for its therapy, liver fibrosis is currently considered to be a major worldwide health problem.

Previous studies have demonstrated that activin A is involved in hepatic fibrosis formation. However, the mechanism of the fibrotic process is not well understood. Activin receptor-interacting protein 2 (ARIP2) has been recently identified as a negative regulator of activin signal pathways. The fact that ARIP2 is highly expressed in the liver suggests that ARIP2 may participate in activin-induced anti-fibrosis in the liver.

A research article published on November 7 in the World Journal of Gastroenterology addresses this question. A research team led by Dr. ZH Liu from Jilin University spent more than five years researching ARIP2. The researchers used mouse Hepal-6 cells obtained from mouse a hepatoma cell line that had functions of hepatic parenchymal cells to investigate the effects of ARIP2 anti-fibrosis on the production of collagen type IV, which is a component of the extracellular matrix (ECM) in liver fibrosis.

One conclusion reported by the investigators is that the mode of expression regulation by various activators of signaling transduction, such as PMA, foskolin and LPS, has been characterized, and its negative effect on the production of collagen type IV revealed, using Hepal-6 cells.

An additional result was that the expression level of ARIP2 mRNA in the Hapel-6 cells was elevated 12 h after treatment with activin A and endotoxin LPS. Thus, it was concluded that ARIP2 participates in the negative feedback regulation of signal transduction in the late stage by affecting the expression of ActRIIA, which further suggests that ARIP2 might be a potential target for treatment of liver fibrosis induced by activin.

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Reference: Zhang HJ, Tai GX, Zhou J, Ma D, Liu ZH. Regulation of activin receptor-interacting protein 2 expression in mouse hepatoma Hepa1-6 cells and its relationship with collagen type IV. World J Gastroenterology 2007; 13(41): 5501-5505

Correspondence to: Professor Zhong-Hui Liu, Department of Immunology, School of Basic Medical Sciences, Jilin University, Changchun 130021, Jilin Province, China.

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection for providing a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th day of every month. The WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Source: You-De Chang
World Journal of Gastroenterology

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