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Involvement of mitochondrial TRPV3 in cardiac hypertrophy induced by pressure overload in rats

ZHU Mei-Ping^1,2, ZHANG Bing-Yi³, LIAN Ting^1,2,4, TAN Yuan-Jia^1,2,5, CHANG Lin-Lin^1,2, XU Pan^1,2,6, ZHANG Jin-Yi^1,2, DU Yan-Huan^1,2, XIONG Zhen-Yu^1,2, DU Qiong⁷, ZHANG Shi-Zhong^1,2,*

¹Third-grade Pharmacological Laboratory on Traditional Chinese Medicine Approved by State Administration of Traditional Chinese Medicine, China Three Gorges University, Yichang 443002, China；²Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, Yichang 443002, China；³Department of Gastroenterology, Yichang Central People’s Hospital, Yichang 443002, China；⁴Department of Gastroenterology, Songzi People’s Hospital, Songzi 434200, China；⁵Department of Pharmacy, Zhijiang People’s Hospital, Zhijiang 443200, China；⁶Investigation School of Jiangxi Police College, Nanchang 330199, China；⁷Department of Neurology, Yiling People’s Hospital of Yichang, Yichang 443002, China

Abstract

Mitochondria play an important role in pressure overload-induced cardiac hypertrophy. The present study aimed to investigate the role of mitochondrial transient receptor potential vanilloid 3 (TRPV3) in myocardial hypertrophy. A 0.7 mm diameter U-shaped silver clip was used to clamp the abdominal aorta of Sprague Dawley (SD) rats and establish an animal model of abdominal aortic constriction (AAC). Rat H9C2 myocardial cells were treated with angiotensin II (Ang II) to establish a hypertrophic myocardial cell model, and TRPV3 expression was knocked down using TRPV3 small interfering RNA (siRNA). JC-1 probe was used to detect mitochondrial membrane potential (MMP). DHE probe was used to detect ROS generation. Enzyme activities of mitochondrial respiratory chain complex I and III and ATP production were detected by assay kits. Immunofluorescence staining was used to detect TRPV3 expression in H9C2 cells. Western blot was used to detect the protein expression levels of β-myosin heavy chain (β-MHC), mitochondrial TRPV3 and mitochondrial NOX4. The results showed that, in the rat AAC model heart tissue and H9C2 cells treated with Ang II, the protein expression levels of β-MHC, mitochondrial TRPV3 and mitochondrial NOX4 were up-regulated, MMP was decreased, ROS generation was increased, mitochondrial respiratory chain complex I and III enzyme activities were decreased, and ATP production was reduced. After knocking down mitochondrial TRPV3 in H9C2 cells, the protein expression levels of β-MHC and mitochondrial NOX4 were down-regulated, MMP was increased, ROS generation was decreased, mitochondrial respiratory chain complex I and III enzyme activities were increased, and ATP production was increased. These results suggest that mitochondrial TRPV3 in cardiomyocytes exacerbates mitochondrial dysfunction by up-regulating NOX4, thereby participating in the process of pressure overload-induced myocardial hypertrophy.

Key words: cardiac hypertrophy; pressure overload; mitochondrion; TRPV3/NOX4

Received: 　　Accepted:

Corresponding author: 张世忠　　E-mail:

Citing This Article：

ZHU Mei-Ping, ZHANG Bing-Yi, LIAN Ting, TAN Yuan-Jia, CHANG Lin-Lin, XU Pan, ZHANG Jin-Yi, DU Yan-Huan, XIONG Zhen-Yu, DU Qiong, ZHANG Shi-Zhong. Involvement of mitochondrial TRPV3 in cardiac hypertrophy induced by pressure overload in rats. Acta Physiol Sin 2024; 76 (5): 703-716