Department of Anatomy and Cell Biology, Faculty of Medicine, University of Sherbrooke, Sherbrooke, QC J1H 5N4, Canada.
Can J Physiol Pharmacol. 2019 Jun;97(6):581-588. doi: 10.1139/cjpp-2018-0592. Epub 2019 Feb 7.
Endocardial endothelial cells (EECs) form a monolayer lining the ventricular cavities. Studies from our laboratory and the literature have shown differences between EECs isolated from the right and left ventricles (EECRs and EECLs, respectively). Angiotensin II (Ang II) was shown to induce apoptosis of different cell types mainly via AT receptor activation. In this study, we verified whether Ang II induces apoptosis of human EECRs and EECLs (hEECRs and hEECLs, respectively) and via which type of receptor. Using the annexin V labeling and in situ TUNEL assays, our results showed that Ang II induced apoptosis of both hEECRs and hEECLs in a concentration-dependent manner. Our results using specific AT and AT receptor antagonists showed that the Ang-II-induced apoptosis in both hEECRs and hEECLs is mediated mainly via the AT receptor. However, AT receptor blockade partially prevented Ang-II-induced apoptosis, particularly in hEECRs. Hence, our results suggest that mainly AT receptors mediate Ang-II-induced apoptosis of hEECRs and hEECLs. The damage of EECs would affect their function as a physical barrier between the blood and cardiomyocytes, thus affecting cardiomyocyte functions.
心内膜内皮细胞 (EECs) 形成一层单层，排列在心室腔的表面。我们实验室和文献中的研究表明，从右心室和左心室分离的 EECs（分别为 EECRs 和 EECLs）之间存在差异。血管紧张素 II (Ang II) 已被证明主要通过 AT 受体激活诱导不同类型细胞的凋亡。在这项研究中，我们验证了 Ang II 是否诱导人 EECRs 和 EECLs（分别为 hEECRs 和 hEECLs）凋亡，以及通过哪种类型的受体。通过 Annexin V 标记和原位 TUNEL 检测，我们的结果表明 Ang II 以浓度依赖性方式诱导 hEECRs 和 hEECLs 凋亡。我们使用特异性 AT 和 AT 受体拮抗剂的结果表明，Ang-II 诱导的 hEECRs 和 hEECLs 凋亡主要通过 AT 受体介导。然而，AT 受体阻断部分阻止了 Ang-II 诱导的 hEECRs 凋亡，尤其是在 hEECRs 中。因此，我们的结果表明，主要是 AT 受体介导 Ang-II 诱导的 hEECRs 和 hEECLs 凋亡。EECs 的损伤会影响它们作为血液和心肌细胞之间物理屏障的功能，从而影响心肌细胞的功能。
