Disruption of the interaction between caveolae and Piezo1 promotes pressure overload-induced cardiac remodeling.

Autor: Li J; Department of Anesthesiology, the Sixth Medical Center of PLA General Hospital, Beijing, 100048, China., Li J; Department of Anesthesiology, the Sixth Medical Center of PLA General Hospital, Beijing, 100048, China., Wu F; Senior Department of Otolaryngology-Head & Neck Surgery, the Sixth Medical Center of PLA General Hospital, Beijing, 100048, China., Yu Z; Department of Anesthesiology, the Sixth Medical Center of PLA General Hospital, Beijing, 100048, China., Yang L; Department of Anesthesiology, the Sixth Medical Center of PLA General Hospital, Beijing, 100048, China. Electronic address: ylyla@hotmail.com.
Jazyk: angličtina
Zdroj: Biochemical and biophysical research communications [Biochem Biophys Res Commun] 2024 Nov 26; Vol. 735, pp. 150456. Date of Electronic Publication: 2024 Jul 26.
DOI: 10.1016/j.bbrc.2024.150456
Abstrakt: Piezo1 channels are activated by mechanical stress and play a significant role in cardiac hypertrophy and fibrosis. However, the molecular mechanisms underlying Piezo1 activation on the cell membrane following pressure overload remain unclear. Caveolae are known to mitigate mechanical forces and regulate Piezo1 function. Therefore, this study aimed to investigate the interaction between caveolae and Piezo1 in the development of pressure overload-induced cardiac remodeling. We observed reduced colocalization between Piezo1 and Caveolin-3 in hypertrophic cardiomyocytes following abdominal aortic constriction and Angiotensin-II treatment, accompanied by increased Piezo1 function and expression. Furthermore, enhanced Piezo1 function was also noted upon caveolae disruption using methyl-beta-cyclodextrin (mβCD). Thus, our findings suggested that pressure overload led to Piezo1 translocation from caveolae, thereby augmenting its function and expression, which may contribute to cardiac remodeling.
Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
(Copyright © 2024 Elsevier Inc. All rights reserved.)
Databáze: MEDLINE
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