Loss of miR-23a cluster in skeletal muscle can suppress bone remodeling

Abstract

exosome, microRNA, muscle-bone interaction, bone remodeling Muscle-bone interaction might regulate bone remodeling in an endocrine manner, but the exact mediators have not been identified. Previous in vitro studies suggest that exosomal miRNAs are a candidate for this interaction. Here we present an in vivo study to show that targeted knockout of a muscle-specific miR-23a cluster including miR-23a, miR-27, and miR-24-2 in skeletal muscle tissues can suppress bone remodeling in mice. The effect of miR-23a cluster seem to not be related to aging, but can worsen the pathological extent of osteoporosis in mice. Our findings suggest that muscle-derived miRNAs may contribute to bone metabolism regulation through exosomes in muscle-bone interaction.

Myoblast-derived exosomal Prrx2 attenuates osteoporosis via transcriptional regulation of lncRNA-MIR22HG to activate Hippo pathway

“…Besides, heat shock proteins (HSP) 25, 70, and 90 were found to be abundant in C2C12 myoblast-derived exosomes (Guescini et al 2010 ), which are essential for osteogenic differentiation (Shimada et al 2003 ; Zhang et al 2018 ). In addition, delivering of muscle-derived exosomal miR-23a cluster could promote bone metabolism (Zhang et al 2021a ). MiR-27a-3p carried by exosomes from C2C12 myoblasts could facilitate pre-osteoblasts MC3T3-E1 differentiation to osteoblasts (Xu et al 2018 ).…”