Medical Scientist Training Program, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Stem Cell Institute, University of Minnesota Medical School, Minneapolis, Minnesota, USA.
Muscle Nerve. 2019 May;59(5):594-602. doi: 10.1002/mus.26433. Epub 2019 Feb 23.
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.
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.
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.
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.
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。
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。
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。
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。
