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Nature Com:miRNA可促进骨骼肌再生

摘要 : 日本京都大学的研究人员发现两种能够促进骨骼肌再生的小核糖核酸,添加了小核糖核酸的骨骼肌干细胞被植入患有肌肉萎缩症的动物体内,可成功实现骨骼肌的再生。相关文章发表于2014年8月14日的《Nature Communications》杂志上。

肌肉萎缩症是一种损坏人体肌肉的遗传性疾病。由于身体无法制造支撑肌肉结构的蛋白质,患者会变得无法运动。目前几乎没有有效的治疗方法。

日本京都大学教授濑原淳子率领的研究小组在调查骨骼肌干细胞保持修复能力的详细机制时,发现向骨骼肌干细胞添加“miR—195”和“miR—497”这两种小核糖核酸后,可以维持骨骼肌干细胞的修复能力。小核糖核酸是一类不编码制造蛋白质的单链核糖核酸分子,主要参与控制基因表达。

研究人员随后将这种骨骼肌干细胞移植到患有肌肉萎缩症的实验鼠腿部,发现腿部的骨骼肌细胞开始增加,肌肉得以再生。

濑原淳子表示,这种方法是否能实现人类骨骼肌细胞的再生还有待研究。如果科学家能利用诱导多功能干细胞(iPS细胞)制作出大批骨骼肌干细胞,就有望用这种方法来预防和治疗肌肉萎缩症。

原文摘要:

miR-195/497 induce postnatal quiescence of skeletal muscle stem cells

Takahiko Sato, Takuya Yamamoto & Atsuko Sehara-Fujisawa

Skeletal muscle stem cells (MuSCs), the major source for skeletal muscle regeneration in vertebrates, are in a state of cell cycle arrest in adult skeletal muscles. Prior evidence suggests that embryonic muscle progenitors proliferate and differentiate to form myofibres and also self-renew, implying that MuSCs, derived from these cells, acquire quiescence later during development. Depletion of ​Dicer in adult MuSCs promoted their exit from quiescence, suggesting microRNAs are involved in the maintenance of quiescence. Here we identified ​miR-195 and ​miR-497 that induce cell cycle arrest by targeting cell cycle genes, Cdc25 and Ccnd. Reduced expression of ​MyoD in juvenile MuSCs, as a result of overexpressed ​miR-195/497 or attenuated Cdc25/Ccnd, revealed an intimate link between quiescence and suppression of myogenesis in MuSCs. Transplantation of cultured MuSCs treated with ​miR-195/497 contributed more efficiently to regenerating muscles of ​dystrophin-deficient mice, indicating the potential utility of ​miR-195/497 for stem cell therapies.

来源: 中国科学报 浏览次数:123

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