ArticleThe Journal of biological chemistry2010
Impairment of transforming growth factor beta signaling in caveolin-1-deficient hepatocytes: role in liver regeneration.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Caveolin-1 Deficiency in Macrophages Alleviates Carbon Tetra-Chloride-Induced Acute Liver Injury in Mice.International journal of molecular sciences · 2025Article
- Review
- Caveolin-1 Modulates Mechanotransduction Responses to Substrate Stiffness through Actin-Dependent Control of YAP.Cell reports · 2018Article
- 3,5-Diethoxy-3'-Hydroxyresveratrol (DEHR) Ameliorates Liver Fibrosis via Caveolin-1 Activation in Hepatic Stellate Cells and in a Mouse Model of Bile Duct Ligation Injury.Molecules (Basel, Switzerland) · 2018Article
- Increased caveolin-1 in intervertebral disc degeneration facilitates repair.Arthritis research & therapy · 2016Article
- Reciprocal regulation of TGF-β and reactive oxygen species: A perverse cycle for fibrosis.Redox biology · 2015Review
- Adipocyte SIRT1 knockout promotes PPARγ activity, adipogenesis and insulin sensitivity in chronic-HFD and obesity.Molecular metabolism · 2015Article
- Plasminogen activator inhibitor-1 suppresses profibrotic responses in fibroblasts from fibrotic lungs.The Journal of biological chemistry · 2015Article
- Caveolin-1 is required for TGF-β-induced transactivation of the EGF receptor pathway in hepatocytes through the activation of the metalloprotease TACE/ADAM17.Cell death & disease · 2014Article
- The less-often-traveled surface of stem cells: caveolin-1 and caveolae in stem cells, tissue repair and regeneration.Stem cell research & therapy · 2013Review
- Eukaryotic elongation factor 2 controls TNF-α translation in LPS-induced hepatitis.The Journal of clinical investigation · 2013Article
- SnoN activates p53 directly to regulate aging and tumorigenesis.Aging cell · 2012Article
- SnoN in regulation of embryonic development and tissue morphogenesis.FEBS letters · 2012Review
- Protein-tyrosine phosphatase 1B (PTP1B) deficiency confers resistance to transforming growth factor-β (TGF-β)-induced suppressor effects in hepatocytes.The Journal of biological chemistry · 2012Article
- Protein Tyrosine Phosphatase 1B (PTP1B) deficiency accelerates hepatic regeneration in mice.The American journal of pathology · 2011Article
- Redox-induced Src kinase and caveolin-1 signaling in TGF-β1-initiated SMAD2/3 activation and PAI-1 expression.PloS one · 2011Article
- SnoN in mammalian development, function and diseases.Current opinion in pharmacology · 2010Review
- Transcriptional cofactors Ski and SnoN are major regulators of the TGF-β/Smad signaling pathway in health and disease.Signal transduction and targeted therapyArticle
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caveolin-1 (Cav-1) is the main structural protein of caveolae and plays an important role in various cellular processes such as vesicular transport, cholesterol homeostasis, and signal transduction pathways. The expression and functional role of Cav-1 have been reported in liver and in hepatocyte cell lines, in human cirrhotic liver, and in hepatocellular carcinomas. Previous studies demonstrated that Cav-1 was dispensable for liver regeneration, because Cav-1(-/-) animals survived and fully regenerated liver function and size after partial hepatectomy. In this study, we have investigated the mechanisms by which the lack of Cav-1 accelerates liver regeneration after partial hepatectomy. The data show that transforming growth factor beta (TGF-beta) signaling is impaired in regenerating liver of Cav-1(-/-) mice and in hepatocytes derived from these animals. TGF-beta receptors I and II do not colocalize in the same membrane fraction in the hepatocytes derived from Cav-1(-/-) mice, as Smad2/3 signaling decreased in the absence of Cav-1 at the time that the transcriptional corepressor SnoN accumulates. Accordingly, the expression of TGF-beta target genes, such as plasminogen activator inhibitor-1, is decreased due to the presence of the high levels of SnoN. Moreover, hepatocyte growth factor inhibited TGF-beta signaling in the absence of Cav-1 by increasing SnoN expression. Taken together, these data might help to unravel why Cav-1-deficient mice exhibit an accelerated liver regeneration after partial hepatectomy and add new insights on the molecular mechanisms controlling the initial commitment to hepatocyte proliferation.
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