ArticleThe Journal of biological chemistry2016
Matrix-driven Myosin II Mediates the Pro-fibrotic Fibroblast Phenotype.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 86 citations in OpenAlex.
- Mechanobiology and Resolution of Lung Fibrosis.Annual review of physiology · 2026Review
- The role of extracellular matrix stiffness in regulating fibroblast behaviors and disease progression.Frontiers in immunology · 2026Review
- Temporal Dynamics of Extracellular Matrix Remodeling in Anthracycline-Induced Cardiotoxicity.Cells · 2025Review
- Depletion of tropomyosin 1.6 alleviates TGF-β1-induced fibroblast activation by promoting the α-SMA-MMP9 matrix-degrading structure.iScience · 2025Article
- Optimal Mechanical Stretch Promotes TSP-1 Expression Through Akt and GSK-3β/β-Catenin Signaling Pathways in Keloid Formation.Health science reports · 2025Article
- Fibroblasts in immune responses, inflammatory diseases and therapeutic implications.Nature reviews. Rheumatology · 2025Review
- Piezo2 Is a Key Mechanoreceptor in Lung Fibrosis that Drives Myofibroblast Differentiation.The American journal of pathology · 2025Article
- Capsule release surgery temporarily reduces contracture in a rat elbow model of arthrofibrosis.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2025Article
- Microvascular endothelial cells display organ-specific responses to extracellular matrix stiffness.Current research in physiology · 2025Article
- Article
- Vimentin is a key regulator of cell mechanosensing through opposite actions on actomyosin and microtubule networks.Communications biology · 2024Article
- Avocado-derived extracellular vesicles loaded with ginkgetin and berberine prevent inflammation and macrophage foam cell formation.Journal of cellular and molecular medicine · 2024Article
- Drebrin is Required for Myosin-facilitated Actin Cytoskeletal Remodeling during Pulmonary Alveolar Development.American journal of respiratory cell and molecular biology · 2024Article
- The role of the cytoskeleton in fibrotic diseases.Frontiers in cell and developmental biology · 2024Review
- Anoctamin-1 is induced by TGF-β and contributes to lung myofibroblast differentiation.American journal of physiology. Lung cellular and molecular physiology · 2024Article
- Implications of Cellular Mechanical Memory in Bioengineering.ACS biomaterials science & engineering · 2023Review
- Anoctamin-1 is induced by TGF-beta and contributes to lung myofibroblast differentiation.bioRxiv : the preprint server for biology · 2023Article
- Actomyosin Activity and Piezo1 Activity Synergistically Drive Urinary System Fibroblast Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Collagen Fibril Orientation Instructs Fibroblast Differentiation Via Cell Contractility.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
Pro-fibrotic mesenchymal cells are known to be the key effector cells of fibroproliferative disease, but the specific matrix signals and the induced cellular responses that drive the fibrogenic phenotype remain to be elucidated. The key mediators of the fibroblast fibrogenic phenotype were characterized using a novel assay system that measures fibroblast behavior in response to actual normal and fibrotic lung tissue. Using this system, we demonstrate that normal lung promotes fibroblast motility and polarization, while fibrotic lung immobilizes the fibroblast and promotes myofibroblast differentiation. These context-specific phenotypes are surprisingly both mediated by myosin II. The role of myosin II is supported by the observation of an increase in myosin phosphorylation and a change in intracellular distribution in fibroblasts on fibrotic lung, as compared with normal lung. Moreover, loss of myosin II activity has opposing effects on protrusive activity in fibroblasts on normal and fibrotic lung. Loss of myosin II also selectively inhibits myofibroblast differentiation in fibroblasts on fibrotic lung. Importantly, these findings are recapitulated by varying the matrix stiffness of polyacrylamide gels in the range of normal and fibrotic lung tissue. Comparison of the effects of myosin inhibition on lung tissue with that of polyacrylamide gels suggests that matrix fiber organization drives the fibroblast phenotype under conditions of normal/soft lung, while matrix stiffness drives the phenotype under conditions of fibrotic/stiff lung. This work defines novel roles for myosin II as a key regulatory effector molecule of the pro-fibrotic phenotype, in response to biophysical properties of the matrix.
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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.