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

IF 1.3 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Xiyang Lu, Guangwei Huang, Hailong Bao, Zonggang Duan, Chao Li, Muzhi Lin, Haiyan Zhou, Zhenhua Luo, Wei Li
{"title":"Effect on hypoxia/reoxygenation-induced cardiomyocyte injury and Pink1/Parkin pathway.","authors":"Xiyang Lu,&nbsp;Guangwei Huang,&nbsp;Hailong Bao,&nbsp;Zonggang Duan,&nbsp;Chao Li,&nbsp;Muzhi Lin,&nbsp;Haiyan Zhou,&nbsp;Zhenhua Luo,&nbsp;Wei Li","doi":"10.4149/gpb_2022045","DOIUrl":null,"url":null,"abstract":"<p><p>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.</p>","PeriodicalId":12514,"journal":{"name":"General physiology and biophysics","volume":"42 1","pages":"87-95"},"PeriodicalIF":1.3000,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"General physiology and biophysics","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.4149/gpb_2022045","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0

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.

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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
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.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信