MicroRNA-125b alleviates hydrogen-peroxide-induced abnormal mitochondrial dynamics in HT22 cells by inhibiting p53

• Published in: Metabolic brain disease Vol. 36; no. 4; pp. 601 - 608
• Main Authors: Huang, Yan, Deng, Songyun, Ai, Yuhang, Mo, Yunan, Li, Wenchao, Peng, Qianyi, Huang, Li, Zhang, Lina
• Format: Journal Article
• Language: English
• Published: New York Springer US 01.04.2021; Springer Nature B.V
• Subjects: Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell death; Damage; Electron microscopy; Hippocampus; Homeostasis; Hydrogen peroxide; Metabolic Diseases; miRNA; Mitochondria; Neurology; Neurosciences; Oncology; Original Article; Oxidative stress; p53 Protein; Oxidative stress; Micro-RNA 125b; Mitochondrial dynamics; p53
• ISSN: 0885-7490; 1573-7365
• DOI: 10.1007/s11011-020-00666-4

Micro-RNA125b (miR-125b) and tumor protein p53 (p53) are involved in the regulation of mitochondrial dynamics; however, the mechanism of their possible interaction during oxidative stress remains unclear. In this study, we investigated the role and mechanism of miR-125b and p53 in oxidative stress-induced mitochondrial damage in immortalized mouse hippocampal HT22 cells. Following stimulation with H 2 O 2 , we observed downregulation of miR-125b expression, upregulation of p53 expression, mitochondria were damaged and increased cell death. Overexpression of miR-125b alleviated mitochondrial damage and inhibited p53 expression. Furthermore, confocal and electron microscopy showed that overexpression of p53 eliminated the protective effect of miR-125b on the mitochondria. Thus, miR-125b alleviates abnormal mitochondrial homeostasis in H 2 O 2 -treated HT22 cells by suppressing p53 expression. Our data reveal a new model by which miR-125b influences mitochondrial dynamics.