ArticleThe Journal of biological chemistry2010
Force-induced myofibroblast differentiation through collagen receptors is dependent on mammalian diaphanous (mDia).
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 32 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
32 citing papers in PubMed, 60 citations in OpenAlex.
- ECM-Stiffness Mediated Persistent Fibroblast Activation Requires Integrin and Formin Dependent Chromatin Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Actin cytoskeleton protection by the formin-mediated safety valve.Current opinion in cell biology · 2025Review
- Activation of an actin signaling pathway in pre-malignant mammary epithelial cells by P-cadherin is essential for transformation.Disease models & mechanisms · 2023Article
- MRTF: Basic Biology and Role in Kidney Disease.International journal of molecular sciences · 2021Review
- Cell Type Dependent Suppression of Inflammatory Mediators by Myocardin Related Transcription Factors.Frontiers in physiology · 2021Article
- Regulation of the Muscarinic MFrontiers in physiology · 2021Article
- Article
- Dynein-mediated nuclear translocation of yes-associated protein through microtubule acetylation controls fibroblast activation.Cellular and molecular life sciences : CMLS · 2020Article
- Article
- Cellular mechanosensing of the biophysical microenvironment: A review of mathematical models of biophysical regulation of cell responses.Physics of life reviews · 2017Review
- Genome-wide DNA methylation analysis in lung fibroblasts co-cultured with silica-exposed alveolar macrophages.Respiratory research · 2017Article
- Molecular networks underlying myofibroblast fate and fibrosis.Journal of molecular and cellular cardiology · 2016Review
- The myofibroblast, a key cell in normal and pathological tissue repair.Cellular and molecular life sciences : CMLS · 2016Review
- Hic-5 is required for myofibroblast differentiation by regulating mechanically dependent MRTF-A nuclear accumulation.Journal of cell science · 2016Article
- Mechanical stimulation induces formin-dependent assembly of a perinuclear actin rim.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- A Role of Myocardin Related Transcription Factor-A (MRTF-A) in Scleroderma Related Fibrosis.PloS one · 2015Article
- Fibroblasts and myofibroblasts in wound healing.Clinical, cosmetic and investigational dermatology · 2014Review
- Formin' cellular structures: Physiological roles of Diaphanous (Dia) in actin dynamics.Communicative & integrative biology · 2013Review
- From tissue mechanics to transcription factors.Differentiation; research in biological diversity · 2013Review
- Strain-induced differentiation of fetal type II epithelial cells is mediated via the integrin α6β1-ADAM17/tumor necrosis factor-α-converting enzyme (TACE) signaling pathway.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The development of fibrosis promotes the differentiation of myofibroblasts, pro-fibrotic cells, which contribute to tissue dysfunction. Myofibroblast differentiation is dependent on actin assembly, which in response to force, is mediated by various actin-binding proteins including the mammalian Diaphanous-related formins (mDia). We examined the role of mDia in the mechano-sensing pathway that leads to force-induced expression of alpha-smooth muscle actin (SMA), a marker and critical determinant of myofibroblast differentiation. In cells treated with siRNA to knockdown mDia and then subjected to tensile force using collagen-coated magnetite beads attached to beta1 integrins, actin assembly was inhibited at bead contact sites. Force-induced nuclear translocation of MRTF-A, a transcriptional co-activator of SMA, was reduced 50% by mDia knockdown. The expression of the transcriptional co-activator of SMA, serum response factor, was reduced by 50% after siRNA knockdown of mDia or by 100% in cells transfected with catalytically inactive mDia. Force-induced activation of the SMA promoter and SMA expression were blocked by knockdown of siRNA of mDia. In anchored collagen gel assays to measure myofibroblast-mediated contraction, knockdown of mDia reduced contraction by 50%. We conclude that mDia plays an important role in the development of force-induced transcriptional activation of SMA and myofibroblast differentiation.
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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.