Effect on hypoxia/reoxygenation-induced cardiomyocyte injury and Pink1/Parkin pathway.

IF 1.3 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY General physiology and biophysics Pub Date : 2023-01-01 DOI:10.4149/gpb_2022045
Xiyang Lu, Guangwei Huang, Hailong Bao, Zonggang Duan, Chao Li, Muzhi Lin, Haiyan Zhou, Zhenhua Luo, Wei Li
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Abstract

Our study aimed to detect the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) on exacerbating cardiomyocyte hypoxia/reoxygenation (H/R) injury and the possible mechanism. A cell model of H/R was constructed. PCSK9 mRNA and protein levels were significantly upregulated during AC16 cardiomyocyte H/R. Flowmetry detection of apoptosis, as well as JC-1, confirmed that PCSK9 upregulation of autophagy levels was accompanied by apoptosis. Furthermore, in the H/R+si-PCSK9 group, the expression of autophagy-related protein LC3 decreased and P62 increased. At the same time, the presentation of the autophagic pathway Pink1/Parkin was also downregulated. In conclusion, in AC16 cardiomyocytes treated with H/R, PCSK9 expression and autophagy levels were increased; a possible molecular mechanism was the activation of the Pink1/Parkin pathway.

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对缺氧/再氧诱导心肌细胞损伤及Pink1/Parkin通路的影响。
本研究旨在检测枯草素/可氧蛋白9型转化酶(PCSK9)对心肌细胞缺氧/再氧化(H/R)损伤的加重作用及其可能的机制。建立H/R细胞模型。在AC16心肌细胞H/R过程中,PCSK9 mRNA和蛋白水平显著上调。流式仪检测细胞凋亡及JC-1,证实PCSK9上调自噬水平伴随细胞凋亡。此外,在H/R+si-PCSK9组中,自噬相关蛋白LC3表达降低,P62表达升高。同时,自噬通路Pink1/Parkin的表达也下调。综上所述,H/R处理后AC16心肌细胞PCSK9的表达和自噬水平升高;可能的分子机制是激活Pink1/Parkin通路。
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来源期刊
General physiology and biophysics
General physiology and biophysics 生物-生化与分子生物学
CiteScore
2.70
自引率
0.00%
发文量
42
审稿时长
6-12 weeks
期刊介绍: General Physiology and Biophysics is devoted to the publication of original research papers concerned with general physiology, biophysics and biochemistry at the cellular and molecular level and is published quarterly by the Institute of Molecular Physiology and Genetics, Slovak Academy of Sciences.
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