Peng Yu, Jingming Ruan, Shaowen Chen, Feng Huang, Pengli Zhu
Provincial Clinical Medical College of Fujian Medical University, Fuzhou 350001, Fujian, China.
Department of Cardiovascular Medicine, Fujian Provincial Hospital South Branch (Fujian Provincial Jinshan Hospital), Fuzhou 350028, Fujian, China.
Iran J Basic Med Sci. 2023 Feb;26(2):183-189. doi: 10.22038/IJBMS.2022.65160.14356.
To determine the protective effect of Apelin-13 on cardiac hypertrophy through activating the PI3K-AKT-mTOR signaling pathway.
The phenylephrine-induced cardiomyocyte hypertrophy model was established in H9C2 cells . Electroporation transfection technology was utilized to prepare and screen the H9C2 cells inducing low expression of the angiotensin type one receptor-related protein (Si-APJ). H9C2 and Si-APJ cells were divided independently into five groups: the control group, the PE group, the PE+Apelin group, the PE+Rapa group, and the PE+Apelin+Rapa group. RT-PCR was performed to analyze the mRNA expression levels of myosin heavy chain 7 (MYH7). Expression of the PI3K/AKT/mTOR pathway proteins and MYH7 was investigated by western blot.
The expression of PI3K/AKT/mTOR phosphorylated proteins was significantly higher in the PE group compared with the PE+Apelin group in H9C2 cells (0.05). Conversely, in Si-APJ H9C2 cells, the expression of PI3K/AKT/mTOR phosphorylated proteins was decreased (0.05). In H9C2 cells, the expression of MYH7 protein was increased in the PE group compared with the control group (0.05). In the same cell line, the expression of MYH7 in the PE+Apelin group was decreased significantly compared with the PE group (0.05). In Si-APJ H9C2 cells, compared with the control group, the expression of MYH7 in the PE group still increased significantly (0.05). In contrast, in the same cell line, there was no statistically significant difference in MYH7 expression between the PE+Apelin, PE+Rapa, and PE+Apelin+Rapa groups compared to the PE group (0.05).
Apelin-13 reduces PE-induced cardiac hypertrophy by activating the PI3K/AKT/mTOR signaling pathway.
通过激活PI3K-AKT-mTOR信号通路来确定Apelin-13对心肌肥大的保护作用。
在H9C2细胞中建立苯肾上腺素诱导的心肌细胞肥大模型。利用电穿孔转染技术制备并筛选诱导血管紧张素1型受体相关蛋白低表达的H9C2细胞（Si-APJ）。将H9C2和Si-APJ细胞分别独立分为五组：对照组、PE组、PE+Apelin组、PE+雷帕霉素组和PE+Apelin+雷帕霉素组。进行逆转录聚合酶链反应（RT-PCR）以分析肌球蛋白重链7（MYH7）的信使核糖核酸（mRNA）表达水平。通过蛋白质免疫印迹法研究PI3K/AKT/mTOR通路蛋白和MYH7的表达。
在H9C2细胞中，PE组中PI3K/AKT/mTOR磷酸化蛋白的表达明显高于PE+Apelin组（P<0.05）。相反，在Si-APJ H9C2细胞中，PI3K/AKT/mTOR磷酸化蛋白的表达降低（P<0.05）。在H9C2细胞中，PE组中MYH7蛋白的表达高于对照组（P<0.05）。在同一细胞系中，PE+Apelin组中MYH7的表达与PE组相比明显降低（P<0.05）。在Si-APJ H9C2细胞中，与对照组相比，PE组中MYH7的表达仍显著增加（P<0.05）。相比之下，在同一细胞系中，与PE组相比，PE+Apelin组、PE+雷帕霉素组和PE+Apelin+雷帕霉素组之间MYH7的表达没有统计学差异（P>0.05）。
Apelin-13通过激活PI3K/AKT/mTOR信号通路减轻PE诱导的心肌肥大。
