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

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

Stem Cells

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

Published: February 2024

AI Article Synopsis

Article Abstract

The expression of large conductance calcium-activated potassium channels (BK channels) in adipose tissue has been identified for years. BK channel deletion can improve metabolism in vivo, but the relative mechanisms remain unclear. Here, we examined the effects of BK channels on the differentiation of adipose-derived stem cells (ADSCs) and the related mechanisms. BKα and β1 subunits were expressed on adipocytes. We found that both deletion of the KCNMA1 gene, encoding the pore forming α subunit of BK channels, and the BK channel inhibitor paxilline increased the expression of key genes in the peroxisome proliferator activated receptor (PPAR) pathway and promoted adipogenetic differentiation of ADSCs. We also observed that the MAPK-ERK pathway participates in BK channel deficiency-promoted adipogenic differentiation of ADSCs and that ERK inhibitors blocked the differentiation-promoting effect of BK channel deficiency. Hyperplasia of adipocytes is considered beneficial for metabolic health. These results indicate that BK channels play an important role in adipose hyperplasia by regulating the differentiation of ADSCs and may become an important target for studying the pathogenesis and treatment strategies of metabolic disorder-related diseases.

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Source
http://dx.doi.org/10.1093/stmcls/sxad082DOI Listing

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