BKCa Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF- β 1/Smad2/3 Signaling Pathways

Zhigui Wu; Wenxian Yin; Mengqi Sun; Yuankai Si; Xiaoxiao Wu; Meijuan Chen

doi:10.1155/2020/3260728

BK_Ca Mediates Dysfunction in High Glucose Induced Mesangial Cell Injury via TGF- β 1/Smad2/3 Signaling Pathways

Int J Endocrinol. 2020 Apr 29:2020:3260728. doi: 10.1155/2020/3260728. eCollection 2020.

Authors

Zhigui Wu¹, Wenxian Yin², Mengqi Sun¹, Yuankai Si¹, Xiaoxiao Wu¹, Meijuan Chen³

Affiliations

¹ Department of Pharmacy, Affiliated Hospital of Southwest Medical University, Luzhou 646000, Sichuan, China.
² Department of Pharmacy, Affiliated Hospital of Traditional Chinese Medicine Southwest Medical University, Luzhou 646000, Sichuan, China.
³ Department of Pharmacy, Southwest Medical University, Luzhou 646000, Sichuan, China.

Abstract

Objective: To explore the role and mechanism of BK_Ca in diabetic kidney disease.

Methods: Rat mesangial cells (MCs) HBZY-1 were cultured with high glucose to simulate the high-glucose environment of diabetic kidney disease in vivo. The effects of large conductance calcium-activated potassium channel (BK_Ca) on proliferation, migration, and apoptosis of HBZY-1 cells were observed. The contents of transforming growth factor beta 1 (TGF-β1), Smad2/3, collagen IV (Col IV), and fibronectin (FN) in the extracellular matrix were also observed.

Results: High glucose significantly damaged HBZY-1 cells, which enhanced the ability of cell proliferation, migration, and apoptosis, and increased the secretion of Col IV and FN. Inhibition of BK_Ca and TGF-β1/Smad2/3 signaling pathways can inhibit the proliferation, migration, and apoptosis of HBZY-1 cells and suppress the secretion of Col IV and FN. The effect of excitation is the opposite.

Conclusions: BK_Ca regulates mesangial cell proliferation, migration, apoptosis, and secretion of Col IV and FN and is associated with TGF-β1/Smad2/3 signaling pathway.