ArticleCell communication and signaling : CCS2018
Selective deletion of hepatocyte platelet-derived growth factor receptor α and development of liver fibrosis in mice.
Article in Cell communication and signaling : CCS, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 23 citations in OpenAlex.
- Mechanisms and reversal strategies of liver fibrosis: from regulation of cell fate to clinical translation.Journal of translational medicine · 2026Review
- Hepatocyte delivery of miR-34b/c reduces hepatic stellate cell activation and improves liver fibrosis.Molecular therapy. Nucleic acids · 2025Article
- Cellular crosstalk mediated by Meteorin-like regulating hepatic stellate cell activation during hepatic fibrosis.Cell death & disease · 2025Article
- Deletion of platelet-derived growth factor receptor β suppresses tumorigenesis in metabolic dysfunction-associated steatohepatitis (MASH) mice with diabetes.Scientific reports · 2024Article
- Spatial Transcriptome Mapping of the Desmoplastic Growth Pattern of Colorectal Liver Metastases by In Situ Sequencing Reveals a Biologically Relevant Zonation of the Desmoplastic Rim.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Article
- Hepatocyte-derived exosomes deliver the lncRNA CYTOR to hepatic stellate cells and promote liver fibrosis.Journal of cellular and molecular medicine · 2024Article
- Potential Application of Small Interfering RNA in Gastro-Intestinal Tumors.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Expression and function of PDGF-C in development and stem cells.Open biology · 2021Review
- Interaction of non‑parenchymal hepatocytes in the process of hepatic fibrosis (Review).Molecular medicine reports · 2021Review
- Lenvatinib prevents liver fibrosis by inhibiting hepatic stellate cell activation and sinusoidal capillarization in experimental liver fibrosis.Journal of cellular and molecular medicine · 2021Article
- Up-regulation of miR-34b/c by JNK and FOXO3 protects from liver fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Liver Fibrosis: Therapeutic Targets and Advances in Drug Therapy.Frontiers in cell and developmental biology · 2021Review
- Liver Fibrosis in Non-alcoholic Fatty Liver Disease: From Liver Biopsy to Non-invasive Biomarkers in Diagnosis and Treatment.Frontiers in medicine · 2021Review
- Erythropoietin Alleviates Burn-induced Muscle Wasting.International journal of medical sciences · 2020Article
- siRNA- and miRNA-based therapeutics for liver fibrosis.Translational research : the journal of laboratory and clinical medicine · 2019Review
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7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPlatelet-derived growth factor receptor α (PDGFRα) expression is increased in activated hepatic stellate cells (HSCs) in cirrhotic liver, while normal hepatocytes express PDGFRα at a negligible level. However, cancerous hepatocytes may show upregulation of PDGFRα, and hepatocellular carcinoma is preceded by chronic liver injury. The role of PDGFRα in non-cancerous hepatocytes and liver fibrosis is unclear. We hypothesized that upon liver injury, PDGFRα in insulted hepatocytes contributes to liver fibrosis by facilitating intercellular crosstalk between hepatocytes and HSCs.
methodsHepatocytes were isolated from normal and thioacetamide (TAA)-induced cirrhotic livers for assessment of PDGFRα expression. Conditional knock-out (KO) C57BL/6 mice, in which PDGFRα was selectively deleted in hepatocytes, were generated. Liver fibrosis was induced by injecting TAA for 8 weeks. Hep3B cells were transfected with a small interfering RNA (siRNA) (PDGFRα or control) and co-cultured with LX2 cells.
resultsPDGFRα expression was increased in hepatocytes from fibrotic livers compared to normal livers. Conditional PDGFRα KO mice had attenuated TAA-induced liver fibrosis with decreased HSC activation and proliferation. Immunoblot analyses revealed decreased expression of phospho-p44/42 MAPK in TAA-treated KO mice; these mice also showed almost complete suppression of the upregulation of mouse double minute 2. Although KO mice exhibited increased expression of transforming growth factor (TGF)-β and Smad2/3, this was compensated for by increased expression of inhibitory Smad7. LX2 cells co-cultured with PDGFRα siRNA-infected Hep3B cells showed decreased PDGFRα, α smooth muscle actin, collagen α1(I), TGFβ, and Smad2/3 expression. LX2/PDGFRα-deleted hepatocyte co-culture medium showed decreased PDGF-BB and PDGF-CC levels.
conclusionsDeletion of PDGFRα in hepatocytes attenuated the upregulation of PDGFRα in HSCs after TAA treatment, resulting in decreased liver fibrosis and HSC activation. This suggests that in the event of chronic liver injury, PDGFRα in hepatocytes plays an important role in liver fibrosis by affecting PDGFRα expression in HSCs.
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