ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2009
Hedgehog pathway activation and epithelial-to-mesenchymal transitions during myofibroblastic transformation of rat hepatic cells in culture and cirrhosis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.
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Who cites it
132 citing papers in PubMed, 219 citations in OpenAlex.
- Therapeutic priming of liver regeneration: from mechanisms toFrontiers in transplantation · 2026Review
- Advances in the treatment of liver injury based on mesenchymal stem cell-derived exosomes.Stem cell research & therapy · 2024Review
- Fibrosis and Hepatocarcinogenesis: Role of Gene-Environment Interactions in Liver Disease Progression.International journal of molecular sciences · 2024Review
- A novel experimental model of MetALD in male mice recapitulates key features of severe alcohol-associated hepatitis.Hepatology communications · 2024Article
- DCDC2 inhibits hepatic stellate cell activation and ameliorates CClScientific reports · 2024Article
- LncRNA-SNHG5 mediates activation of hepatic stellate cells by regulating NF2 and Hippo pathway.Communications biology · 2024Article
- Identification of a distal enhancer regulating hedgehog interacting protein gene in human lung epithelial cells.EBioMedicine · 2024Article
- Circular RNA cVIM promotes hepatic stellate cell activation in liver fibrosis via miR-122-5p/miR-9-5p-mediated TGF-β signaling cascade.Communications biology · 2024Article
- Review
- Mechanism and Progress of Natural Products in the Treatment of NAFLD-Related Fibrosis.Molecules (Basel, Switzerland) · 2023Review
- Knockdown of Yap attenuates TAA-induced hepatic fibrosis by interaction with hedgehog signals.Journal of cell communication and signaling · 2023Article
- Placenta mesenchymal stem cell-derived extracellular vesicles alleviate liver fibrosis by inactivating hepatic stellate cells through a miR-378c/SKP2 axis.Inflammation and regeneration · 2023Article
- Indian Hedgehog release from TNF-activated renal epithelia drives local and remote organ fibrosis.Science translational medicine · 2023Article
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- ALS-L1023 fromLife (Basel, Switzerland) · 2022Article
- Hepatic Stellate Cell-Immune Interactions in NASH.Frontiers in endocrinology · 2022Review
- Therapeutic Effects of Berberine on Liver Fibrosis are associated With Lipid Metabolism and Intestinal Flora.Frontiers in pharmacology · 2022Review
- The Role of the Hedgehog Pathway in Cholangiocarcinoma.Cancers · 2021Review
- Regulatory long non-coding RNAs of hepatic stellate cells in liver fibrosis (Review).Experimental and therapeutic medicine · 2021Review
- Hepatectomy-Induced Alterations in Hepatic Perfusion and Function - Toward Multi-Scale Computational Modeling for a Better Prediction of Post-hepatectomy Liver Function.Frontiers in physiology · 2021Review
72 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 5 institutions in 1 country.
Funding
Abstract
Myofibroblastic hepatic stellate cells (MF-HSC) are derived from quiescent hepatic stellate cells (Q-HSC). Q-HSC express certain epithelial cell markers and have been reported to form junctional complexes similar to epithelial cells. We have shown that Hedgehog (Hh) signaling plays a key role in HSC growth. Because Hh ligands regulate epithelial-to-mesenchymal transition (EMT), we determined whether Q-HSC express EMT markers and then assessed whether these markers change as Q-HSC transition into MF-HSC and whether the process is modulated by Hh signaling. Q-HSC were isolated from healthy livers and cultured to promote myofibroblastic transition. Changes in mRNA and protein expression of epithelial and mesenchymal markers, Hh ligands, and target genes were monitored in HSC treated with and without cyclopamine (an Hh inhibitor). Studies were repeated in primary human HSC and clonally derived HSC from a cirrhotic rat. Q-HSC activation in vitro (culture) and in vivo (CCl(4)-induced cirrhosis) resulted in decreased expression of Hh-interacting protein (Hhip, an Hh antagonist), the EMT inhibitors bone morphogenic protein (BMP-7) and inhibitor of differentiation (Id2), the adherens junction component E-cadherin, and epithelial keratins 7 and 19 and increased expression of Gli2 (an Hh target gene) and mesenchymal markers, including the mesenchyme-associated transcription factors Lhx2 and Msx2, the myofibroblast marker alpha-smooth muscle actin, and matrix molecules such as collagen. Cyclopamine reverted myofibroblastic transition, reducing mesenchymal gene expression while increasing epithelial markers in rodent and human HSC. We conclude that Hh signaling plays a key role in transition of Q-HSC into MF-HSC. Our findings suggest that Q-HSC are capable of transitioning between epithelial and mesenchymal fates.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.