ArticleDigestive diseases and sciences2012
Gene transfer of c-met confers protection against D-galactosamine/lipopolysaccharide-induced acute liver failure.
Article in Digestive diseases and sciences, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 19 citations in OpenAlex.
- Genetic modification of mesenchymal stem cells (MSCs): novel strategy to expand their naïve applications in critical illness.Molecular biology reports · 2025Review
- Potential advantages of genetically modified mesenchymal stem cells in the treatment of acute and chronic liver diseases.Stem cell research & therapy · 2023Review
- Genetically Modified Mesenchymal Stromal/Stem Cells: Application in Critical Illness.Stem cell reviews and reports · 2020Review
- Pre-treatments enhance the therapeutic effects of mesenchymal stem cells in liver diseases.Journal of cellular and molecular medicine · 2020Review
- Progress in mesenchymal stem cell-based therapy for acute liver failure.Stem cell research & therapy · 2018Review
- Review
- Overexpression of c-Met in bone marrow mesenchymal stem cells improves their effectiveness in homing and repair of acute liver failure.Stem cell research & therapy · 2017Article
- Mechanistic Modelling of Drug-Induced Liver Injury: Investigating the Role of Innate Immune Responses.Gene regulation and systems biology · 2017Article
- [Role of autophagy in acute liver failure induced by D-galactosamine/lipopolysaccharide in mice].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2016Article
- Image-Guided Hydrodynamic Gene Delivery: Current Status and Future Directions.Pharmaceutics · 2015Review
- In vivo siRNA delivery of Keap1 modulates death and survival signaling pathways and attenuates concanavalin-A-induced acute liver injury in mice.Disease models & mechanisms · 2014Article
- Mest attenuates CCl4-induced liver fibrosis in rats by inhibiting the Wnt/β-catenin signaling pathway.Gut and liver · 2014Article
- Sustained endoplasmic reticulum stress inhibits hepatocyte proliferation via downregulation of c-Met expression.Molecular and cellular biochemistry · 2014Article
- PKCα signaling pathway involves in TNF-α-induced IP3R1 expression in human mesangial cells.World journal of emergency medicine · 2012Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAcute liver failure (ALF) is characterized by impaired regeneration of hepatocytes, partially resulting from the defective signaling between elevated levels of hepatocyte growth factor (HGF) and the downregulation of its receptor, c-met.
aimsIn this study, we assess the therapeutic efficacy of in vivo c-met gene transfer in ALF.
methodsWe established a D: -galactosamine/lipopolysaccharide (D: -GalN/LPS)-induced ALF model in rats. The levels of HGF and c-met in D: -GalN/LPS rats were compared with vehicle-injected rats and those undergoing liver regeneration following partial hepatectomy (PH). To deliver c-met in vivo, pcDNA-c-met was constructed and transfected into the rat liver via hydrodynamic injection. Control rats were transfected with the pcDNA3.1 plasmid. The expressions of c-met in different tissues were examined by immunohistochemistry. Hepatocyte proliferation and apoptosis were determined by PCNA staining and TUNEL assay, respectively. The survival of rats in the control and c-met-expressing rats was compared by Kaplan-Meier analysis.
resultsCompared with control rats, D: -GalN/LPS or PH -treated rats had significantly higher levels of HGF (P < 0.01). D: -GalN/LPS also led to significantly lower c-met expression in the liver (P < 0.01) than PH. The in vivo c-met gene transfer led to its specific expression on hepatocytes, which was accompanied by the enhancement of hepatocyte proliferation, a reduction in apoptosis, as well as significant improvement in overall survival (P < 0.01).
conclusionsThis study provides the initial evidence that c-met may serve as a novel target for gene therapy, and may be of clinical benefit in the treatment of patients with ALF.
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