Myonectin inhibits the differentiation of osteoblasts and osteoclasts in mouse cells

Miku Kawaguchi1, Naoyuki Kawao1, Yoshimasa Takafuji1

  • 1Department of Physiology and Regenerative Medicine, Kindai University Faculty of Medicine, 377-2 Ohnohigashi, Osakasayama, Osaka, 589-8511, Japan.

Heliyon
|June 10, 2020
PubMed

Insights

Myonectin, a myokine, inhibits osteoblast differentiation and activity. It also suppresses osteoclast formation by impacting mitochondrial biogenesis, revealing its role in bone health.

Area of Science:

  • Bone Biology
  • Endocrinology
  • Skeletal Muscle Physiology

Background:

  • Myonectin is a myokine implicated in diabetes and obesity.
  • Myokines mediate skeletal muscle and bone interactions.
  • The specific role of myonectin in bone physiology remains largely unexplored.

Purpose of the Study:

  • To investigate the effects of myonectin on osteoblast differentiation.
  • To examine the impact of myonectin on osteoclastogenesis.
  • To elucidate the mechanisms underlying myonectin's influence on bone cells.

Main Methods:

  • In vitro studies using mouse osteoblasts and RAW264.7 cells.
  • Assessment of osteogenic gene expression and alkaline phosphatase (ALP) activity.
  • Analysis of osteoclast formation and related gene expression induced by RANKL.
  • Evaluation of mitochondrial biogenesis parameters, including oxygen consumption rate.

Main Results:

  • Myonectin significantly suppressed osteoblast differentiation markers and ALP activity.
  • Myonectin inhibited RANKL-induced osteoclast formation and associated gene expression.
  • Myonectin reduced mitochondrial biogenesis in RAW264.7 cells, affecting oxygen consumption and PGC-1β levels.
  • These mitochondrial effects were not observed in osteoblasts.

Conclusions:

  • Myonectin negatively regulates osteoblast differentiation and activity.
  • Myonectin impairs osteoclast differentiation, partly via inhibition of mitochondrial biogenesis.
  • These findings highlight myonectin as a potential regulator of bone metabolism.