抑制 microRNA-92a 增加骨骼肌中的血管和卫星细胞，但不能改善 mdx 小鼠与杜氏肌营养不良症相关的表型。
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.
机构信息
Medical Scientist Training Program, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Stem Cell Institute, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
出版信息
Muscle Nerve. 2019 May;59(5):594-602. doi: 10.1002/mus.26433. Epub 2019 Feb 23.
INTRODUCTION
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.
简介
杜氏肌营养不良症（DMD）及其 mdx 小鼠模型中的肌肉血管和血流受到干扰。微 RNA-92a（miR-92a）在血管内皮细胞中丰富，特别是在缺血损伤期间。
方法
因为拮抗 miR-92a 会导致内皮细胞增殖和迁移增加，并从缺血中恢复，所以我们在肌肉干细胞培养物中评估了 Antagomir-92a 的体外作用，在 mdx 小鼠中评估了其体内作用。
结果
miR-92a 在肌肉内皮细胞和卫星细胞中高度表达。用 Antagomir-92a 处理可增加毛细血管密度和组织灌注，同时增加卫星细胞。然而，用 Antagomir-92a 处理的 mdx 小鼠没有显示出组织学改善，肌肉功能更差。Antagomir-92a 抑制了卫星细胞培养物中的成肌分化。
讨论
AntagomiR-92a 改善了 mdx 小鼠的血管系统，但没有改善肌肉，可能是因为它对卫星细胞分化有副作用。肌肉神经 59:594-594，2019 年。
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