{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,19]],"date-time":"2026-01-19T11:07:26Z","timestamp":1768820846873,"version":"3.49.0"},"reference-count":45,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2019,2,23]],"date-time":"2019-02-23T00:00:00Z","timestamp":1550880000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100005202","name":"Muscular Dystrophy Association","doi-asserted-by":"publisher","award":["MDA 241600"],"award-info":[{"award-number":["MDA 241600"]}],"id":[{"id":"10.13039\/100005202","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["F30AR066454"],"award-info":[{"award-number":["F30AR066454"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000069","name":"National Institute of Arthritis and Musculoskeletal and Skin Diseases","doi-asserted-by":"publisher","award":["NIH1R03AR061545"],"award-info":[{"award-number":["NIH1R03AR061545"]}],"id":[{"id":"10.13039\/100000069","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Muscle and Nerve"],"published-print":{"date-parts":[[2019,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p><jats:italic>Introduction<\/jats:italic>: The vasculature and blood flow in muscle are perturbed in Duchenne muscular dystrophy (DMD) and its <jats:italic>mdx<\/jats:italic> mouse model. MicroRNA\u201092a (miR\u201092a) is enriched in endothelial cells, especially during ischemic injury. <jats:italic>Methods<\/jats:italic>: Because antagonizing miR\u201092a was shown to result in increased proliferation and migration of endothelial cells and recovery from ischemia, we assessed the effects of Antagomir\u201092a <jats:italic>in vitro<\/jats:italic> in muscle stem cell culture and <jats:italic>in vivo<\/jats:italic> in <jats:italic>mdx<\/jats:italic> mice. <jats:italic>Results<\/jats:italic>: miR\u201092a was found to be highly expressed in muscle endothelial cells and satellite cells. Treatment with Antagomir\u201092a increased capillary density and tissue perfusion, which was accompanied by an increase in satellite cells. However, Antagomir\u201092a\u2013treated <jats:italic>mdx<\/jats:italic> mice showed no histological improvement and had worse muscle function. Antagomir\u201092a suppressed myogenic differentiation in satellite cell culture. <jats:italic>Discussion<\/jats:italic>: AntagomiR\u201092a improves the vasculature but not the muscle in <jats:italic>mdx<\/jats:italic> mice, possibly due to its side effects on satellite cell differentiation. <jats:italic>Muscle Nerve<\/jats:italic> 59:594\u2013594, 2019<\/jats:p>","DOI":"10.1002\/mus.26433","type":"journal-article","created":{"date-parts":[[2019,1,30]],"date-time":"2019-01-30T11:38:53Z","timestamp":1548848333000},"page":"594-602","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Inhibition of microRNA\u201092a increases blood vessels and satellite cells in skeletal muscle but does not improve duchenne muscular dystrophy\u2013related phenotype in <i>mdx<\/i> 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