ArticleWound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society
Whole animal knockout of smooth muscle alpha-actin does not alter excisional wound healing or the fibroblast-to-myofibroblast transition.
Article in Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 50 citations in OpenAlex.
- Evaluation of esthetic outcome of delayed implants with de-epithelialized free gingival graft in thin gingival phenotype with or without immediate temporization: a randomized clinical trial.International journal of implant dentistry · 2023Trial
- Actin cytoskeletal dynamics in hepatic myofibroblasts and fibrosis.Nature reviews. Gastroenterology & hepatology · 2026Review
- Fibroblast and myofibroblast activation in normal tissue repair and fibrosis.Nature reviews. Molecular cell biology · 2024Review
- The Role of Myofibroblasts in Physiological and Pathological Tissue Repair.Cold Spring Harbor perspectives in biology · 2023Review
- Loss of Acta2 in cardiac fibroblasts does not prevent the myofibroblast differentiation or affect the cardiac repair after myocardial infarction.Journal of molecular and cellular cardiology · 2022Article
- Dermal αSMAThe EMBO journal · 2022Article
- Wound healing: cellular mechanisms and pathological outcomes.Open biology · 2020Review
- Knockdown of CK2α reducesInternational journal of medical sciences · 2020Article
- Smooth Muscle α-Actin Deficiency Leads to Decreased Liver Fibrosis via Impaired Cytoskeletal Signaling in Hepatic Stellate Cells.The American journal of pathology · 2019Article
- Article
- Wound Healing: A Cellular Perspective.Physiological reviews · 2019Review
- CD44-dependent inflammation, fibrogenesis, and collagenolysis regulates extracellular matrix remodeling and tensile strength during cutaneous wound healing.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Impaired Contracture of 3D Collagen Constructs by Fibronectin-Deficient Murine Fibroblasts.Frontiers in physiology · 2019Article
- Reactive Oxygen Species and NOX Enzymes Are Emerging as Key Players in Cutaneous Wound Repair.International journal of molecular sciences · 2017Review
- Regeneration of injured skin and peripheral nerves requires control of wound contraction, not scar formation.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2017Review
- Article
- Matrix-driven Myosin II Mediates the Pro-fibrotic Fibroblast Phenotype.The Journal of biological chemistry · 2016Article
- Myofibroblasts contribute to but are not necessary for wound contraction.Laboratory investigation; a journal of technical methods and pathology · 2015Article
- A biomechanical perspective on stress fiber structure and function.Biochimica et biophysica acta · 2015Review
- Article
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4 authors at 3 institutions in 1 country.
Funding
Abstract
The contractile phenotype and function of myofibroblasts have been proposed to play a critical role in wound closure. It has been hypothesized that smooth muscle α-actin expressed in myofibroblasts is critical for its formation and function. We have used smooth muscle α-actin-null mice to test this hypothesis. Full-thickness excisional wounds closed at a similar rate in smooth muscle α-actin-null and wild-type mice. In addition, fibroblasts in smooth muscle α-actin-null granulation tissue when immunostained with a monoclonal antibody that recognizes all muscle actin isoforms exhibited a myofibroblast-like distribution and a stress fiber-like pattern, showing that these cells acquired the myofibroblast phenotype. Dermal fibroblasts from smooth muscle α-actin-null and wild-type mice formed stress fibers and supermature focal adhesions, and generated similar amounts of contractile force in response to transforming growth factor-β1. Smooth muscle γ-actin and skeletal muscle α-actin were expressed in smooth muscle α-actin-null myofibroblasts, as shown by immunostaining, real-time polymerase chain reaction, and mass spectrometry. These results show that smooth muscle α-actin is not necessary for myofibroblast formation and function and for wound closure, and that smooth muscle γ-actin and skeletal muscle α-actin may be able to functionally compensate for the lack of smooth muscle α-actin in myofibroblasts.
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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.