Abstract

Myonectin is a myokine, which is involved in the pathophysiology of diabetes and obesity, and various myokines are involved in the interactions between skeletal muscle and bone. However, roles of myonectin in bone have still remained unknown. We therefore examined the effects of myonectin on mouse osteoblast and osteoclast differentiation in vitro. Myonectin significantly suppressed the mRNA levels of osteogenic genes and alkaline phosphatase (ALP) activity in mouse osteoblasts. As for osteoclasts, myonectin significantly suppressed osteoclast formation as well as the mRNA levels of osteoclast-related genes enhanced by receptor activator nuclear factor κB ligand (RANKL) from mouse monocytic RAW264.7 cells. Moreover, myonectin significantly suppressed osteoclast formation from mouse bone marrow cells in the presence of macrophage-colony stimulating factor and RANKL. On the other hand, myonectin significantly suppressed RANKL-induced oxygen consumption rate and peroxisome proliferator-activated receptor γ coactivator-1β mRNA levels in RAW264.7 cells, although myonectin did not affect these mitochondrial biogenesis parameters in mouse osteoblasts. In conclusion, the present study demonstrated that myonectin suppresses the differentiation and ALP activity in mouse osteoblasts. Moreover, myonectin suppressed osteoclast differentiation from mouse bone marrow and RAW264.7 cells partly through an inhibition of mitochondrial biogenesis.

Highlights

  • Myokines are factors secreted from the skeletal muscles, and many myokines play some roles in metabolic regulation through the circulation during physical exercise

  • It suppressed osteoclast differentiation from mouse bone marrow and RAW264.7 cells, the effects of myonectin on bone resorbing activity of osteoclasts have still remained unknown in the present study

  • These findings suggest that myonectin might be involved in the interactions between muscle and bone in the pathophysiology of osteoporosis

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Summary

Introduction

Myokines are factors secreted from the skeletal muscles, and many myokines play some roles in metabolic regulation through the circulation during physical exercise. Myonectin induced in erythroblasts links stress erythropoiesis to iron mobilization in liver in response to blood loss in mice [10], and Otaka et al recently reported that myonectin improves myocardiac injury through a reduction in cardiac myocyte apoptosis and macrophage-related inflammation in mice [11]. These findings suggest that myonectin is an important myokine for the regulation of metabolic state. Roles of myonectin in bone have still remained unknown

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