ArticleJournal of cell science2016
Hic-5 is required for myofibroblast differentiation by regulating mechanically dependent MRTF-A nuclear accumulation.
Article in Journal of cell science, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed.
- Hic-5 drives epithelial mechanotransduction promoting a feed-forward cycle of bronchoconstriction.Nature communications · 2025Article
- Engineering an Injectable Scaffold with Enhanced ECM Mimicry for Cell Delivery and Tissue Regeneration.ACS biomaterials science & engineering · 2025Article
- The role of multi-omics in biomarker discovery, diagnosis, prognosis, and therapeutic monitoring of tissue repair and regeneration processes.Journal of orthopaedic translation · 2025Review
- HBI-8000 improves heart failure with preserved ejection fraction via the TGF-β1/MAPK signalling pathway.Journal of cellular and molecular medicine · 2024Article
- Anatomical Anal Stenosis after PPH: Insights from a Retrospective Study and Rat Model.International journal of molecular sciences · 2024Article
- Hic-5 regulates extracellular matrix-associated gene expression and cytokine secretion in cancer associated fibroblasts.Experimental cell research · 2024Article
- Molecular and metabolomic characterization of hiPSC-derived cardiac fibroblasts transitioning to myofibroblasts.Frontiers in cell and developmental biology · 2024Article
- Heterogeneous response to TGF-β1/3 isoforms in fibroblasts of different origins: implications for wound healing and tumorigenesis.Histochemistry and cell biology · 2023Article
- Knockdown of mechanosensitive adaptor Hic-5 ameliorates post-traumatic osteoarthritis in rats through repression of MMP-13.Scientific reports · 2023Article
- The Role of Myofibroblasts in Physiological and Pathological Tissue Repair.Cold Spring Harbor perspectives in biology · 2023Review
- Relieving DYRK1A repression of MKL1 confers an adult-like phenotype to human infantile megakaryocytes.The Journal of clinical investigation · 2022Article
- Contribution of Endothelial Laminin-Binding Integrins to Cellular Processes Associated with Angiogenesis.Cells · 2022Article
- Click-functionalized hydrogel design for mechanobiology investigations.Molecular systems design & engineering · 2021Article
- Myofibroblasts: Function, Formation, and Scope of Molecular Therapies for Skin Fibrosis.Biomolecules · 2021Review
- Integrin α4β1 is required for IL-1α- and Nrf2-dependent, Cox-2 induction in fibroblasts, supporting a mechanism that suppresses α-SMA expression.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2021Article
- Discovery and validation of novel protein markers in mucosa of portal hypertensive gastropathy.BMC gastroenterology · 2021Article
- Suppression of MKL1 promotes adipocytic differentiation and reduces the proliferation of myxoid liposarcoma cells.Oncology letters · 2020Article
- Exploring microRNAs in diabetic chronic cutaneous ulcers: Regulatory mechanisms and therapeutic potential.British journal of pharmacology · 2020Review
- Hypertrophic Scarring: Current Knowledge of Predisposing Factors, Cellular and Molecular Mechanisms.Journal of burn care & research : official publication of the American Burn Association · 2020Review
- Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.International review of cell and molecular biology · 2020Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
How mechanical cues from the extracellular environment are translated biochemically to modulate the effects of TGF-β on myofibroblast differentiation remains a crucial area of investigation. We report here that the focal adhesion protein, Hic-5 (also known as TGFB1I1), is required for the mechanically dependent generation of stress fibers in response to TGF-β. Successful generation of stress fibers promotes the nuclear localization of the transcriptional co-factor MRTF-A (also known as MKL1), and this correlates with the mechanically dependent induction of α smooth muscle actin (α-SMA) and Hic-5 in response to TGF-β. As a consequence of regulating stress fiber assembly, Hic-5 is required for the nuclear accumulation of MRTF-A and the induction of α-SMA as well as cellular contractility, suggesting a crucial role for Hic-5 in myofibroblast differentiation. Indeed, the expression of Hic-5 was transient in acute wounds and persistent in pathogenic scars, and Hic-5 colocalized with α-SMA expression in vivo. Taken together, these data suggest that a mechanically dependent feed-forward loop, elaborated by the reciprocal regulation of MRTF-A localization by Hic-5 and Hic-5 expression by MRTF-A, plays a crucial role in myofibroblast differentiation in response to TGF-β.
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