2. Academic Validation
  3. BK Channel Deficiency in Osteoblasts Reduces Bone Formation via the Wnt/β-Catenin Pathway

BK Channel Deficiency in Osteoblasts Reduces Bone Formation via the Wnt/β-Catenin Pathway

  • Mol Cells. 2021 Aug 31;44(8):557-568. doi: 10.14348/molcells.2021.0004.
Lan Jiang 1 2,  Qianhong Yang 1 2,  Jianjun Gao 3,  Jiahong Yang 1,  Jiaqi He 1,  Hong Xin 1 4,  Xuemei Zhang 1
Affiliations

Affiliations

  • 1 Department of Pharmacology, School of Pharmacy & Minhang Hospital, Fudan University, Shanghai 201203, China.
  • 2 These authors contributed equally to this work.
  • 3 Department of Bone Metabolism, Institute of Radiation Medicine, Fudan University, Shanghai 200032, China.
  • 4 shanghai Zhangjiang Institute of Medical Innovation, Shanghai 201204, China.
PMID: 34385407 DOI: 10.14348/molcells.2021.0004
Abstract

Global knockout of the BK channel has been proven to affect bone formation; however, whether it directly affects osteoblast differentiation and the mechanism are elusive. In the current study, we further investigated the role of BK channels in bone development and explored whether BK channels impacted the differentiation and proliferation of osteoblasts via the canonical Wnt signaling pathway. Our findings demonstrated that knockout of Kcnma1 disrupted the osteogenesis of osteoblasts and inhibited the stabilization of β-catenin. Western blot analysis showed that the protein levels of Axin1 and USP7 increased when Kcnma1 was deficient. Together, this study confirmed that BK ablation decreased bone mass via the Wnt/β-catenin signaling pathway. Our findings also showed that USP7 might have the ability to stabilize the activity of Axin1, which would increase the degradation of β-catenin in osteoblasts.

Keywords

BK channel; Kcnma1; bone development; osteoblasts; β-catenin.

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