ArticleGastroenterology2012
Fibronectin extra domain-A promotes hepatic stellate cell motility but not differentiation into myofibroblasts.
Article in Gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 50 citations in OpenAlex.
- Single-cell insights into hepatic fibroblasts and stellate cells: heterogeneity in matrix remodelling in development, health, and disease.Npj gut and liver · 2026Review
- Liver Fibrosis: Interactions Between Cells and Microenvironments.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2025Review
- Article
- Liver sinusoidal endothelial cells as potential drivers of liver fibrosis (Review).Molecular medicine reports · 2024Article
- A roadmap for developing and engineeringBiophysics reviews · 2023Review
- Tissue mechanics coevolves with fibrillar matrisomes in healthy and fibrotic tissues.Matrix biology : journal of the International Society for Matrix Biology · 2022Review
- Proteomic Changes of Activated Hepatic Stellate Cells.International journal of molecular sciences · 2021Article
- Adipocyte Fatty Acid Binding Protein Promotes the Onset and Progression of Liver Fibrosis via Mediating the Crosstalk between Liver Sinusoidal Endothelial Cells and Hepatic Stellate Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021Article
- Design and Evaluation of a Polypeptide that Mimics the Integrin Binding Site for EDA Fibronectin to Block Profibrotic Cell Activity.International journal of molecular sciences · 2021Article
- Integrin-α9β1 as a Novel Therapeutic Target for Refractory Diseases: Recent Progress and Insights.Frontiers in immunology · 2021Review
- FN-EDA mediates angiogenesis of hepatic fibrosis via integrin-VEGFR2 in a CD63 synergetic manner.Cell death discovery · 2020Article
- Proteasomal Degradation of Enhancer of Zeste Homologue 2 in Cholangiocytes Promotes Biliary Fibrosis.Hepatology (Baltimore, Md.) · 2019Article
- The fibronectin ED-A domain enhances recruitment of latent TGF-β-binding protein-1 to the fibroblast matrix.Journal of cell science · 2018Article
- Biology of portal hypertension.Hepatology international · 2018Review
- Signaling Mechanisms of Myofibroblastic Activation: Outside-in and Inside-Out.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Review
- Liver Sinusoidal Endothelial Cell: An Update.Seminars in liver disease · 2017Review
- Matrix Remodeling in Pulmonary Fibrosis and Emphysema.American journal of respiratory cell and molecular biology · 2016Review
- Identification and characterization of a unique role for EDB fibronectin in phagocytosis.Journal of molecular medicine (Berlin, Germany) · 2016Article
- Stuck in the Middle: Fibronectin-Binding Proteins in Gram-Positive Bacteria.Frontiers in microbiology · 2016Review
- Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsMyofibroblasts are the primary cell type involved in physiologic wound healing and its pathologic counterpart, fibrosis. Cellular fibronectin that contains the alternatively spliced extra domain A (EIIIA) is up-regulated during these processes and is believed to promote myofibroblast differentiation. We sought to determine the requirement for EIIIA in fibrosis and differentiation of myofibroblasts in rodent livers.
methodsWe used a mechanically tunable hydrogel cell culture system to study differentiation of primary hepatic stellate cells and portal fibroblasts from rats into myofibroblasts. Liver fibrosis was induced in mice by bile duct ligation or administration of thioacetamide.
resultsEIIIA was not required for differentiation of rat hepatic stellate cells or portal fibroblasts into fibrogenic myofibroblasts. Instead, hepatic stellate cells cultured on EIIIA-containing cellular fibronectin formed increased numbers of lamellipodia; their random motility and chemotaxis also increased. These increases required the receptor for EIIIA, the integrin α(9)β(1). In contrast, the motility of portal fibroblasts did not increase on EIIIA, and these cells expressed little α(9)β(1). Male EIIIA(-/-) mice were modestly protected from thioacetamide-induced fibrosis, which requires motile hepatic stellate cells, but not from bile duct ligation-induced fibrosis, in which portal fibroblasts are more important. Notably, myofibroblasts developed during induction of fibrosis with either thioacetamide or bile duct ligation in EIIIA(-/-) mice.
conclusionsEIIIA is dispensable for differentiation of hepatic stellate cells and portal fibroblasts to myofibroblasts, both in culture and in mouse models of fibrosis. Our findings, however, indicate a role for EIIIA in promoting stellate cell motility and parenchymal liver fibrosis.
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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.