Lmod3 promotes myoblast differentiation and proliferation via the AKT and ERK pathways

Fei-Hu Lin1, Anmin Wang2, Wuhou Dai3

  • 1State Key Laboratory of Genetic Engineering and National Center for International Research of Development and Disease, Fudan-Yale Center for Biomedical Research, Innovation Center for International Cooperation of Genetics and Development, Institute of Developmental Biology and Molecular Medicine, School of Life Sciences, Children's Hospital of Fudan University, Fudan University, Shanghai, China.

Experimental Cell Research
|September 27, 2020
PubMed

Insights

The Lmod3 gene is crucial for muscle cell development. This study shows Lmod3 (Leucine-rich repeat-containing protein 3) promotes muscle cell differentiation and proliferation via AKT and ERK signaling pathways.

Area of Science:

  • Muscle biology
  • Cellular signaling
  • Genetics

Background:

  • Mutations in the Lmod3 gene are linked to nemaline myopathy.
  • The precise function of Lmod3 and its role in muscle disease pathogenesis are not well understood.

Purpose of the Study:

  • To investigate the role of Lmod3 in myoblast differentiation and proliferation.
  • To elucidate the signaling pathways involved in Lmod3-mediated muscle cell regulation.

Main Methods:

  • Utilized C2C12 myoblast cell line.
  • Performed Lmod3 knockdown and overexpression experiments.
  • Assessed myoblast differentiation, proliferation, and apoptosis.
  • Analyzed AKT and ERK signaling pathway activation.
  • Investigated the effect of IGF-1 administration.

Main Results:

  • Lmod3 knockdown inhibited myoblast differentiation and proliferation, and induced apoptosis.
  • Lmod3 overexpression enhanced myoblast differentiation and proliferation.
  • Lmod3 modulated the activation of AKT and ERK pathways during differentiation and proliferation, respectively.
  • IGF-1 partially rescued the negative effects of Lmod3 knockdown.

Conclusions:

  • Lmod3 plays a significant role in promoting myoblast differentiation and proliferation.
  • The AKT and ERK signaling pathways are key mediators of Lmod3's function in muscle cells.
  • Lmod3 is a potential therapeutic target for muscle-related disorders.

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