ArticleMedical science monitor : international medical journal of experimental and clinical research2012
Coexpression of Smad7 and UPA attenuates carbon tetrachloride-induced rat liver fibrosis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- SimulatedPostepy dermatologii i alergologii · 2022Article
- Effect of medicated serum ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017Article
- Article
- Human urokinase-type plasminogen activator gene-modified bone marrow-derived mesenchymal stem cells attenuate liver fibrosis in rats by down-regulating the Wnt signaling pathway.World journal of gastroenterology · 2016Article
- Activity of MMP1 and MMP13 and amino acid metabolism in patients with alcoholic liver cirrhosis.Medical science monitor : international medical journal of experimental and clinical research · 2015Article
- miR-33a levels in hepatic and serum after chronic HBV-induced fibrosis.Journal of gastroenterology · 2015Article
- Astragalus and Paeoniae Radix Rubra extract (APE) inhibits hepatic stellate cell activation by modulating transforming growth factor-β/Smad pathway.Molecular medicine reports · 2015Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThere is a great need for developing novel therapies to treat liver fibrosis. Previous studies showed that both Smad7 and uPA were inhibitors of liver fibrosis. Therefore, we explored the therapeutic effects of combinational gene therapy with Smad7 and uPA on CCl4-induced liver fibrosis. MATERIAL/
methodsSmad7 and uPA genes were cloned into an adenovirus vector. To observe the therapeutic effects of coexpression of Smad7 and uPA genes, the recombinant adenovirus were delivered into CCL4-induced fibrosis models. Fibrillar collagen, hydroxyproline, α-SMA, TGF-β1, MMP-13, TIMP-1, HGF and PCNA were detected to evaluate the fibrosis and to explore the mechanisms underlying the treatment with Smad7 and uPA.
resultsThe results showed that single Smad7 or uPA adenovirus reduced CCL4 induced liver fibrosis significantly; while combination of Smad7 and uPA had more significant therapeutic effect on CCl4 induced liver fibrosis. Then the markers underlying the therapeutic effect of combination of Smad7 and uPA were also explored. Over-expression of Smad7 and uPA inhibited the expression of α-SMA and TGF- β1 significantly. Combinational gene therapy also enhanced extracellular matrix degradation by increasing the expression of MMP-13, inhibiting TIMP-1 expression, and promoted hepatocyte proliferation, while single Smad7 or uPA only induced part of these changes.
conclusionsThese results suggest that combinational gene therapy with Smad7 and uPA inhibited CCl4-induced rat liver fibrosis by simultaneously targeting multiple pathogenic pathways.
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