ArticleThe Journal of biological chemistry2014
Activated hepatic stellate cells are dependent on self-collagen, cleaved by membrane type 1 matrix metalloproteinase for their growth.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.
- High throughput interrogation of human liver stellate cells reveals microenvironmental regulation of phenotype.Acta biomaterialia · 2022Pooled it
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Development of novel nucleic acid therapy aimed at directly controlling liver fibrosis.Molecular therapy. Nucleic acids · 2025Article
- Mmp14-dependent remodeling of the pericellular-dermal collagen interface governs fibroblast survival.The Journal of cell biology · 2024Article
- The protective effects of Ninjin'yoeito against liver steatosis/fibrosis in a non-alcoholic steatohepatitis model mouse.Journal of natural medicines · 2024Article
- Tumor necrosis factor-inducible gene 6 protein and its derived peptide ameliorate liver fibrosis by repressing CD44 activation in mice with alcohol-related liver disease.Journal of biomedical science · 2024Article
- Fibrosis Regression After Eradication of Hepatitis C Virus: From Bench to Bedside.Gastroenterology · 2021Review
- Emerging strategies to disrupt the central TGF-β axis in kidney fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
- The Expanding Role of MT1-MMP in Cancer Progression.Pharmaceuticals (Basel, Switzerland) · 2019Review
- Autocrine CTHRC1 activates hepatic stellate cells and promotes liver fibrosis by activating TGF-β signaling.EBioMedicine · 2019Article
- Current status, problems, and perspectives of non-alcoholic fatty liver disease research.World journal of gastroenterology · 2019Review
- Hepatic stellate cells derived from the nestin-positive cells in septum transversum during rat liver development.Medical molecular morphology · 2018Article
- Endoplasmic reticulum oxidase 1α is critical for collagen secretion from and membrane type 1-matrix metalloproteinase levels in hepatic stellate cells.The Journal of biological chemistry · 2017Article
- CREB3L2-mediated expression of Sec23A/Sec24D is involved in hepatic stellate cell activation through ER-Golgi transport.Scientific reports · 2017Article
- Genetic and epigenetic regulation of intestinal fibrosis.United European gastroenterology journal · 2016Review
- Involvement of Pancreatic Stellate Cells in Regeneration of Remnant Pancreas after Partial Pancreatectomy.PloS one · 2016Article
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stellate cells are distributed throughout organs, where, upon chronic damage, they become activated and proliferate to secrete collagen, which results in organ fibrosis. An intriguing property of hepatic stellate cells (HSCs) is that they undergo apoptosis when collagen is resolved by stopping tissue damage or by treatment, even though the mechanisms are unknown. Here we disclose the fact that HSCs, normal diploid cells, acquired dependence on collagen for their growth during the transition from quiescent to active states. The intramolecular RGD motifs of collagen were exposed by cleavage with their own membrane type 1 matrix metalloproteinase (MT1-MMP). The following evidence supports this conclusion. When rat activated HSCs (aHSCs) were transduced with siRNA against the collagen-specific chaperone gp46 to inhibit collagen secretion, the cells underwent autophagy followed by apoptosis. Concomitantly, the growth of aHSCs was suppressed, whereas that of quiescent HSCs was not. These in vitro results are compatible with the in vivo observation that apoptosis of aHSCs was induced in cirrhotic livers of rats treated with siRNAgp46. siRNA against MT1-MMP and addition of tissue inhibitor of metalloproteinase 2 (TIMP-2), which mainly inhibits MT1-MMP, also significantly suppressed the growth of aHSCs in vitro. The RGD inhibitors echistatin and GRGDS peptide and siRNA against the RGD receptor αVβ1 resulted in the inhibition of aHSCs growth. Transduction of siRNAs against gp46, αVβ1, and MT1-MMP to aHSCs inhibited the survival signal of PI3K/AKT/IκB. These results could provide novel antifibrosis strategies.
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Registered trials
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