Journal
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY
Volume 60, Issue 4, Pages 262-268Publisher
SAGE PUBLICATIONS LTD
DOI: 10.1369/0022155412438104
Keywords
liver fibrosis; decorin; small leucine-rich proteoglycan; TGF-beta 1; extracellular matrix; hepatic stellate cells
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Funding
- Hungarian Scientific Research Fund [67925, 100904]
- National Institutes of Health [RO1 CA39481]
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Hepatic fibrosis and cirrhosis are worldwide health care problems, especially in regions with a high rate of hepatitis infection. As these diseases affect a major part of the human population, the search for antifibrotic therapies has a high priority in medical research. Transforming growth factor beta 1 (TGF-beta 1) is one of the most powerful profibrotic cytokines. Thus, blocking TGF-beta 1 activity by natural inhibitors represents a valid and logical strategy to combat hepatic fibrosis. One of the natural inhibitors of TGF-beta 1 is decorin, a small leucine-rich proteoglycan that binds with high affinity to this cytokine and prevents its interaction with pro-fibrotic receptors. Recent evidence has shown that decorin has a protective role in liver fibrogenesis insofar as its genetic ablation in mice leads to enhanced matrix deposition, impaired matrix degradation, and activation of hepatic stellate cells, the main producers of fibrotic tissue. Moreover, TGF-beta 1 exerts a stronger effect when functional decorin is absent. These data provide robust genetic evidence for a direct role of endogenous decorin in preventing and retarding hepatic fibrosis. Thus, boosting the endogenous production of decorin or systemic delivery of recombinant decorin could represent an additional therapeutic modality against hepatic fibrosis.(J Histochem Cytochem 60: 262-268, 2012)
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