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Pb inhibited C2C12 myoblast differentiation by regulating HDAC2

Xiaozhen Gu1, Nan Shen1, Chengqing Huang1

  • 1Engineering Research Center of Bio-process, Ministry of Education, Hefei University of Technology, 193 Tunxi Road, Hefei, Anhui 230009, PR China; School of Food and Biological Engineering, Hefei University of Technology, No. 193 of Tunxi Road, Baohe District, 230009 Hefei, China.

Toxicology
|October 5, 2023
PubMed

Insights

Lead exposure harms skeletal muscle development by inhibiting C2C12 myoblast differentiation. This process is mediated by the epigenetic regulator histone deacetylase-2 (HDAC2), highlighting a novel toxicity pathway.

Area of Science:

  • Cell Biology
  • Toxicology
  • Developmental Biology

Background:

  • Myogenesis is vital for skeletal muscle development and homeostasis.
  • Lead (Pb) exposure negatively impacts bone health, particularly in children.
  • The specific effects of lead on skeletal muscle development remain largely unknown.

Purpose of the Study:

  • To investigate the toxic effects of lead (Pb) on C2C12 myoblast proliferation and differentiation.
  • To elucidate the role of histone deacetylase-2 (HDAC2) in Pb-induced inhibition of myogenesis.

Main Methods:

  • C2C12 myoblasts were exposed to varying concentrations of Pb (1, 5, and 10 μM).
  • Cell viability assays were performed to assess Pb toxicity.
  • Myogenic differentiation markers (MCK, MYH4, MYOG, MYOD) and HDAC2 expression were analyzed.
  • HDAC2 knockdown was employed to determine its role in Pb-induced differentiation deficits.

Main Results:

  • Pb exposure at 5 μM and 10 μM significantly decreased C2C12 cell viability.
  • Pb exposure (1-10 μM) markedly inhibited myoblast differentiation, reducing key myogenic marker gene expression.
  • Lead exposure led to the upregulation of histone deacetylase-2 (HDAC2) in C2C12 myoblasts.
  • Knockdown of HDAC2 partially rescued the Pb-induced inhibition of C2C12 myoblast differentiation.

Conclusions:

  • Lead exposure inhibits skeletal muscle development by impairing C2C12 myoblast differentiation.
  • The epigenetic modifier histone deacetylase-2 (HDAC2) plays a critical role in mediating Pb-induced myogenesis deficits.
  • These findings reveal a novel mechanism of lead toxicity impacting skeletal muscle development.
Keywords:
HDAC2Myoblasts differentiationPbProliferation

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