Angiotensin II prompts heart cell apoptosis via AT1 receptor-augmented phosphatase and tensin homolog and miR-320-3p functions to enhance suppression of the IGF1R-PI3K-AKT survival pathway. Issue 12 (31st December 2022)

• Record Type: Journal Article
• Authors: Lu, Shang-Yeh; Hong, Wei-Zhi; Tsai, Bruce Chi-Kang; Chang, Yu-Chun; Kuo, Chia-Hua; Mhone, Thomas G.; Chen, Ray-Jade; Kuo, Wei-Wen; Huang, Chih-Yang
• Is Part Of: Journal of hypertension. Volume 40:Issue 12(2022)
• Page Start: 2502
• Page End: 2512
• Publication Date: 2022-12-31
• Subjects: angiotensin II -- heart damage -- hypertension -- mir-320 -- phosphatase and tensin homolog -- renin–angiotensin–aldosterone system; Hypertension -- Periodicals; Hypertension -- Periodicals; 616.132005
• DOI: 10.1097/HJH.0000000000003285
• Languages: English
• ISSNs: 1473-5598

Abstract

Abstract : Background: Hypertension is a severe public health risk factor worldwide. Elevated angiotensin II (Ang II) produced by the renin–angiotensin–aldosterone system can lead to hypertension and its complications. Method: In this study, we addressed the cardiac-injury effects of Ang II and investigated the signaling mechanism induced by Ang II. Both H9c2 cardiomyoblast cells and neonatal rat cardiomyocytes were exposed to Ang II to observe hypertension-related cardiac apoptosis. Results: The results of western blotting revealed that Ang II significantly attenuated the IGF1R-PI3K-AKT pathway via the Ang II-AT1 receptor axis and phosphatase and tensin homolog expression. Furthermore, real-time PCR showed that Ang II also activated miR-320-3p transcription to repress the PI3K-Akt pathway. In the heart tissue of spontaneously hypertensive rats, activation of the IGF1R survival pathway was also reduced compared with that in Wistar-Kyoto rats, especially in aged spontaneously hypertensive rats. Conclusion: Hence, we speculate that the Ang II-AT1 receptor axis induces both phosphatase and tensin homolog and miR-320-3p expression to downregulate the IGF1R-PI3K-AKT survival pathway and cause cell apoptosis in the heart.