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BK Channel Depletion Promotes Adipocyte Differentiation by Activating the MAPK/ERK Pathway

Fang Xin1,2, Yuan Cheng1, Xinxin Wen1

  • 1Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Youanmenwai, Beijing 100069, People's Republic of China.

Stem Cells (Dayton, Ohio)
|November 12, 2023
PubMed

Insights

Large conductance calcium-activated potassium (BK) channels regulate adipose-derived stem cell differentiation. Blocking BK channels promotes adipogenesis, offering potential therapeutic targets for metabolic disorders.

Area of Science:

  • Biochemistry
  • Cell Biology
  • Metabolic Science

Background:

  • Large conductance calcium-activated potassium (BK) channels are expressed in adipose tissue.
  • BK channel deletion improves metabolism, but mechanisms are unclear.

Purpose of the Study:

  • To investigate BK channel effects on adipose-derived stem cell (ADSC) differentiation.
  • To elucidate the molecular mechanisms underlying BK channel influence on adipogenesis.

Main Methods:

  • Examined BK channel (BKα and β1 subunits) expression in adipocytes.
  • Utilized KCNMA1 gene deletion and paxilline inhibition.
  • Assessed gene expression in the peroxisome proliferator activated receptor (PPAR) pathway.
  • Investigated the involvement of the MAPK-ERK pathway.

Main Results:

  • KCNMA1 deletion and paxilline increased PPAR pathway gene expression and promoted ADSC adipogenic differentiation.
  • The MAPK-ERK pathway mediates BK channel deficiency-promoted adipogenesis.
  • ERK inhibitors counteracted the differentiation-promoting effects of BK channel deficiency.

Conclusions:

  • BK channels regulate ADSC differentiation and adipose tissue hyperplasia.
  • BK channels represent a potential therapeutic target for metabolic disorders.
Keywords:
BK channelsERKMAPKadipose-derived stem cellshyperplasiainduction of differentiation

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