ArticleMolecular medicine (Cambridge, Mass.)2011
Angiotensin-II mediates nonmuscle myosin II activation and expression and contributes to human keloid disease progression.
Article in Molecular medicine (Cambridge, Mass.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Enhanced Scar Reduction Using Topical Application of Captopril-containing Silicone Gel in a Rabbit Model of Hypertrophic Scars.International journal of medical sciences · 2026Article
- Pleiotrophin modulates cell proliferation, prostate smooth muscle contraction and fibrosis in hyperplastic prostate.Journal of translational medicine · 2025Article
- AT2R Activation Improves Wound Healing in a Preclinical Mouse Model.Biomedicines · 2024Article
- Dysregulated myosin in Hermansky-Pudlak syndrome lung fibroblasts is associated with increased cell motility.Respiratory research · 2022Article
- Angiotensin-Converting Enzyme Inhibitor, Captopril, Improves Scar Healing in Hypertensive Rats.International journal of medical sciences · 2021Article
- Nonmuscle Myosin II Activation Regulates Cell Proliferation, Cell Contraction, and Myofibroblast Differentiation in Keloid-Derived Fibroblasts.Advances in wound care · 2020Article
- Effect of donor non-muscle myosin heavy chain (MYH9) gene polymorphisms on clinically relevant kidney allograft dysfunction.BMC nephrology · 2020Article
- Pre-vascularization Enhances Therapeutic Effects of Human Mesenchymal Stem Cell Sheets in Full Thickness Skin Wound Repair.Theranostics · 2017Article
- Angiotensin II stimulates canonical TGF-β signaling pathway through angiotensin type 1 receptor to induce granulation tissue contraction.Journal of molecular medicine (Berlin, Germany) · 2015Article
- Admixture mapping identifies a locus at 15q21.2-22.3 associated with keloid formation in African Americans.Human genetics · 2014Article
- A novel immune competent murine hypertrophic scar contracture model: a tool to elucidate disease mechanism and develop new therapies.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Aberrant fibroblast migration in response to fibrogenic peptides plays a significant role in keloid pathogenesis. Angiotensin II (Ang II) is an octapeptide hormone recently implicated as a mediator of organ fibrosis and cutaneous repair. Ang II promotes cell migration but its role in keloid fibroblast phenotypic behavior has not been studied. We investigated Ang II signaling in keloid fibroblast behavior as a potential mechanism of disease. Primary human keloid fibroblasts were stimulated to migrate in the presence of Ang II and Ang II receptor 1 (AT₁), Ang II receptor 2 (AT₂) or nonmuscle myosin II (NMM II) antagonists. Keloid and the surrounding normal dermis were immunostained for NMM IIA, NMM IIB, AT₂ and AT₁ expression. Primary human keloid fibroblasts were stimulated to migrate with Ang II and the increased migration was inhibited by the AT₁ antagonist EMD66684, but not the AT₂ antagonist PD123319. Inhibition of the promigratory motor protein NMM II by addition of the specific NMM II antagonist blebbistatin inhibited Ang II-stimulated migration. Ang II stimulation of NMM II protein expression was prevented by AT₁ blockade but not by AT₂ antagonists. Immunostaining demonstrated increased NMM IIA, NMM IIB and AT₁ expression in keloid fibroblasts compared with scant staining in normal surrounding dermis. AT₂ immunostaining was absent in keloid and normal human dermal fibroblasts. These results indicate that Ang II mediates keloid fibroblast migration and possibly pathogenesis through AT₁ activation and upregulation of NMM II.
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