过表达miR-29ab1簇通过抑制Mstn导致1月龄小鼠肌肉过度生长。

IF 4.6 Q2 MATERIALS SCIENCE, BIOMATERIALS
Chuncheng Liu, Yuxin Cao, Lei Li, Yiting Wang, Qingyong Meng
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引用次数: 0

摘要

骨骼肌质量与力量和健康密切相关。骨骼肌肥大的调控涉及多种基因和信号通路。miR-29可以通过不同的靶基因参与骨骼肌发育的各种过程。然而,还需要研究miR-29在小鼠青春期骨骼肌中的功能。我们使用在骨骼肌内特异性诱导miR-29ab1簇过表达的小鼠,研究了1月龄时miR-29过表达对骨骼肌的影响。我们发现在幼年小鼠中miR-29ab1簇的过表达导致骨骼肌质量和肌纤维横截面积增加。对miR-29诱导骨骼肌肥大机制的研究发现,miR-29是通过抑制Mstn的表达来实现其功能的。同时,在过表达miR-29ab1簇的骨骼肌中存在损伤的肌纤维。骨骼肌的损伤可能与miR-29对IV型胶原的抑制有关。这些结果表明,miR-29ab1簇的过表达虽然可以诱导幼鼠骨骼肌肥大,但同时也会引起骨骼肌损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Overexpression of miR-29ab1 Cluster Results in Excessive Muscle Growth in 1-Month-old Mice by Inhibiting Mstn.
Skeletal muscle mass is closely related to strength and health. Multiple genes and signaling pathways are involved in the regulation of skeletal muscle hypertrophy. miR-29 can participate in various processes of skeletal muscle development through different target genes. However, studies are needed on the function of miR-29 in skeletal muscle during mouse puberty. We used mice in which overexpression of miR-29ab1 cluster could be induced specifically within skeletal muscle, and investigated the effects of miR-29 overexpression on skeletal muscle at 1 month of age. We found that the overexpression of miR-29ab1 cluster in juvenile mice caused skeletal muscle mass and myofiber cross-sectional area to increase. The study on the mechanism of miR-29 inducing skeletal muscle hypertrophy had found that miR-29 achieved its function by inhibiting the expression of Mstn. At the same time, injured myofibers were present within miR-29ab1 cluster overexpressing skeletal muscle. The damage of skeletal muscle may be due to the inhibition of the type IV collagen by miR-29. These results indicate that although the overexpression of miR-29ab1 cluster can induce skeletal muscle hypertrophy in mouse juvenile, it simultaneously causes skeletal muscle damage.
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来源期刊
ACS Applied Bio Materials
ACS Applied Bio Materials Chemistry-Chemistry (all)
CiteScore
9.40
自引率
2.10%
发文量
464
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