关键词:

低温缺氧/复氧, 心肌成纤维细胞, H9c2细胞, 缝隙连接蛋白43, 细胞间通讯

Abstract:

Objective To observe the effect on myocardial H9c2 cells gap junction intercellular communi⁃ cation（GJIC）by rat cardiac fibroblasts（RCFs）after hypothermia hypoxia/reoxygen（H/R）and to explore the pos⁃ sible mechanisms. Methods After co⁃cultured of RCFs cells with H9c2 cells in a 2:1 number ratio by Transwell， cells was randomly divided into 6 groups. The T+AngⅡ group and H/R⁃T+AngⅡ group were added 1.5nM AngⅡ， and the T+ARB group and H/R⁃T+ARB group were added 1nM valsartan. The T group，T+AngⅡ group and T+ ARB group were cultured normally，and the H/R⁃T group，H/R⁃T+AngⅡ and H/R⁃T+ARB group were treated with H/R. The AngⅡ concentration in the culture medium；the expression and phosphorylation of Cx43 and ERK1/2； and GJIC of H9c2 cells were detected. Results Compared with the T group，the expression and phosphorylation of ERK1/2 and Cx43 were decreased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in the H/R⁃T and T+Ang II group; he expression and phosphorylation of ERK1/2 and Cx43 were increased（P < 0.05）and GJIC was enhanced（P < 0.05）in H9c2 cells in the T+ARB group. Compared with H/R ⁃T group，he expression and phosphorylation of ERK1/2 and Cx43 were decreased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in H/R ⁃T+Ang II group; and the expression and phosphorylation of ERK1/2 and Cx43 were increased（P < 0.05）and GJIC was diminished（P < 0.05）in H9c2 cells in H/R ⁃T+ARB group. Conclusion After H/R，in⁃ creased AngⅡ secretion by RCFs may downregulate Cx43 expression by inhibiting the MAPK/ERK pathway in H9c2 cells，resulting in diminished GJIC between H9c2 cells.

Key words:

hypothermia hypoxia/reoxygenation, cardiac fibroblasts, H9c2 cells, connexin 43, gap junction intercellular communication