Lu Xiyang, Huang Guangwei, Bao Hailong, Duan Zonggang, Li Chao, Lin Muzhi, Zhou Haiyan, Luo Zhenhua, Li Wei
Department of Cardiovascular Medicine, The Affiliated Hospital of Guizhou Medical University, Guiyang, Guizhou, China.
Gen Physiol Biophys. 2023 Jan;42(1):87-95. doi: 10.4149/gpb_2022045.
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.
我们的研究旨在检测前蛋白转化酶枯草杆菌蛋白酶/克新蛋白酶9型（PCSK9）对加剧心肌细胞缺氧/复氧（H/R）损伤的影响及其可能机制。构建了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。流式细胞术检测凋亡以及JC-1证实，PCSK9上调自噬水平伴有凋亡。此外，在H/R+si-PCSK9组中，自噬相关蛋白LC3表达降低，P62增加。同时，自噬途径Pink1/Parkin的表达也下调。总之，在用H/R处理的AC16心肌细胞中，PCSK9表达和自噬水平升高；一种可能的分子机制是Pink1/Parkin途径的激活。
