Regulation of H9C2 cell hypertrophy by 14-3-3η via inhibiting glycolysis.

Autor: Wan S; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China., Wang S; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China., Yang X; Guangxi Key Laboratory of Brain and Cognitive Neuroscience, Guilin Medical University, Guilin, China., Cui Y; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China.; Clinical Pathology Department, The Second People's Hospital of Yichang, Yichang, China., Guan H; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China., Xiao W; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China., Liu F; Department of Anatomy, College of Basic Medicine, Guilin Medical University, Guilin, China.; Center of Diabetic Systems Medicine, Guangxi Key Laboratory of Excellence, Guilin Medical University, Guilin, China.
Jazyk: angličtina
Zdroj: PloS one [PLoS One] 2024 Jul 22; Vol. 19 (7), pp. e0307696. Date of Electronic Publication: 2024 Jul 22 (Print Publication: 2024).
DOI: 10.1371/journal.pone.0307696
Abstrakt: It has been reported that Ywhah (14-3-3η) reduces glycolysis. However, it remains unclear about the downstream mechanism by which glycolysis is regulated by 14-3-3η in cardiac hypertrophy. As an important regulator, Yes-associated protein (YAP) interacts with 14-3-3η to participate in the initiation and progression of various diseases in vivo. In this study, the model of H9C2 cardiomyocyte hypertrophy was established by triiodothyronine (T3) or rotenone stimulation to probe into the action mechanism of 14-3-3η. Interestingly, the overexpression of 14-3-3η attenuated T3 or rotenone induced cardiomyocyte hypertrophy and decreased glycolysis in H9C2 cardiomyocytes, whereas the knockdown of 14-3-3η had an opposite effect. Mechanistically, 14-3-3η can reduce the expression level of YAP and bind to it to reduce its nuclear translocation. In addition, changing YAP may affect the expression of lactate dehydrogenase A (LDHA), a glycolysis-related protein. Meanwhile, LDHA is also a possible target for 14-3-3η to mediate glycolysis based on changes in pyruvate, a substrate of LDHA. Collectively, 14-3-3η can suppress cardiomyocyte hypertrophy via decreasing the nucleus translocation of YAP and glycolysis, which indicates that 14-3-3η could be a promising target for inhibiting cardiac hypertrophy.
Competing Interests: The authors have declared that no competing interests exist.
(Copyright: © 2024 Wan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
Databáze: MEDLINE
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