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Adipose-derived exosomes ameliorate skeletal muscle atrophy via miR-146a-5p/IGF-1R signaling

文献类型: 外文期刊

作者: Qin, Mengran 1 ; Zhu, Jiahao 1 ; Xing, Lipeng 1 ; Fan, Yaotian 1 ; Luo, Junyi 1 ; Sun, Jiajie 1 ; Chen, Ting 1 ; Zhang, Yongliang 1 ; Xi, Qianyun 1 ;

作者机构: 1.South China Agr Univ, Guangdong Prov Key Lab Anim Nutr Control, State Key Lab Livestock & Poultry Breeding, Natl Engn Res Ctr Breeding Swine Ind,Coll Anim Sci, 483 Wushan Rd, Guangzhou 510642, Peoples R China

2.Tianjin Univ, Tianjin Hosp, Tianjin 300211, Peoples R China

3.Tianjin Orthoped Inst, Tianjin Key Lab Orthoped Biomech & Med Engn, Tianjin 300050, Peoples R China

关键词: Muscle atrophy; IGF-1R; Exosomes; miR-146a-5p; Skeletal muscle; Adipose

期刊名称:JOURNAL OF NANOBIOTECHNOLOGY ( 影响因子:12.6; 五年影响因子:12.3 )

ISSN:

年卷期: 2024 年 22 卷 1 期

页码:

收录情况: SCI

摘要: The study of muscle disorders has gained popularity, with a particular emphasis on the relationship between adipose tissue and skeletal muscle. In our investigation, we discovered that the deletion of miR-146a-5p specifically in adipose tissue (aKO) led to a notable rise in mice's mass and adiposity. In contrast, it led to a decline in lean mass, ability to exercise, diameter of muscle fibers, and the levels of genes associated with differentiation. The co-culture experiment showed that the transfection of miR-146a-5p mimics to 3T3-L1 significantly suppressive cell growth and promotes myotube differentiation in C2C12 cells. Exosomes from white adipose tissue (WAT) of aKO mice (aKO-WAT-Exos) significantly promoted muscle atrophy and inhibited differentiation of C2C12 cells but were reversed by co-incubation with miR-146a-5p-mimics. The miR-146a-5p can specifically target IGF-1R to improve skeletal muscle wasting. In this process, the PI3K/AKT/mTOR pathway is activated or the FoxO3 pathway is inhibited to enhance the synthesis of skeletal muscle proteins. Significantly, miR-146a-5p serves a crucial function as a microRNA in the communication of the fat-muscle connection. It can be transported through the pathway of exosomes derived from adipose tissue, ultimately ameliorating skeletal muscle atrophy and modulating body mass index (BMI).

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