Home General Physiology and Biophysics 2023 General Physiology and Biophysics Vol.42, No.4, p. 349–360, 2023

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.42, No.4, p. 349–360, 2023

Title: BST-1 aggravates aldosterone-induced cardiac hypertrophy via the Ca2+/CaN/NFATc3 pathway
Author: Yao Yuan, Lina Zhao, Hongjuan Cao, Sha Li, Chunyan Liao, Lei Fu, Xing Wang, Fuqin Huang, Weidan Zeng, Aiyue Li, Bei Zhang

Abstract: BST-1 (bone marrow stromal cell antigen-1) is thought to be a key molecule involved in regulating the functional activity of cells in various tissues and organs. BST-1 can catalyze the hydrolysis of nicotinamide adenine dinucleotide (NAD+) to produce cyclic ADP ribose (cADPR), which activates the activity of intracellular Ca2+ signaling. Currently, the role of BST-1 regulation of Ca2+ signaling pathway in pathological myocardial hypertrophy is unclear. We found elevated expression of BST-1 in cardiac hypertrophy tissues of spontaneously hypertensive rats in our vivo study, subsequently; the mechanism of BST-1 action on myocardial hypertrophy was explored in vitro experiment. We used aldosterone (ALD) to induce H9C2 cellular hypertrophy. cADPR levels and intracellular Ca2+ concentrations declined and calcium-regulated neurophosphatase (CaN) activity and protein expression were decreased after BST-1 knockdown. And then activated T-cell nuclear factor (NFATc3) entry nucleus was inhibited. All of the above resulted in that H9C2 cells size was reduced by rhodamine-phalloidin staining. Thus, BST-1 may exacerbate cardiac hypertrophy by activating the Ca2+/CaN/NFATc3 pathway.

Keywords: BST-1 — Cardiac hypertrophy — CaN — NFATc3 — Aldosterone
Published online: 03-Jul-2023
Year: 2023, Volume: 42, Issue: 4 Page From: 349, Page To: 360

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