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Inhibition of microRNA‐92a increases blood vessels and satellite cells in skeletal muscle but does not improve duchenne muscular dystrophy–related phenotype in mdx mice
Author(s) -
Verma Mayank,
Asakura Yoko,
Asakura Atsushi
Publication year - 2019
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.26433
Subject(s) - duchenne muscular dystrophy , antagomir , stem cell , skeletal muscle , muscular dystrophy , medicine , myocyte , pathology , biology , anatomy , endocrinology , microrna , microbiology and biotechnology , biochemistry , gene
: The vasculature and blood flow in muscle are perturbed in Duchenne muscular dystrophy (DMD) and its mdx mouse model. MicroRNA‐92a (miR‐92a) is enriched in endothelial cells, especially during ischemic injury. Methods : Because antagonizing miR‐92a was shown to result in increased proliferation and migration of endothelial cells and recovery from ischemia, we assessed the effects of Antagomir‐92a in vitro in muscle stem cell culture and in vivo in mdx mice. Results : miR‐92a was found to be highly expressed in muscle endothelial cells and satellite cells. Treatment with Antagomir‐92a increased capillary density and tissue perfusion, which was accompanied by an increase in satellite cells. However, Antagomir‐92a–treated mdx mice showed no histological improvement and had worse muscle function. Antagomir‐92a suppressed myogenic differentiation in satellite cell culture. Discussion : AntagomiR‐92a improves the vasculature but not the muscle in mdx mice, possibly due to its side effects on satellite cell differentiation. Muscle Nerve 59:594–594, 2019