MFN2型
细胞生物学
褪黑素
线粒体融合
线粒体
第一季
DNM1L型
活力测定
品脱1
生物
活性氧
线粒体生物发生
MFN1型
细胞凋亡
化学
线粒体DNA
线粒体分裂
细胞
生物化学
粒体自噬
内分泌学
自噬
基因
作者
Maria Gemma Nasoni,Silvia Carloni,Barbara Canonico,Sabrina Burattini,Erica Cesarini,Stefano Papa,Marica Pagliarini,Patrizia Ambrogini,Walter Balduini,Francesca Luchetti
摘要
Mitochondrial dysfunction is considered one of the hallmarks of ischemia/reperfusion injury. Mitochondria are plastic organelles that undergo continuous biogenesis, fusion, and fission. They can be transferred between cells through tunneling nanotubes (TNTs), dynamic structures that allow the exchange of proteins, soluble molecules, and organelles. Maintaining mitochondrial dynamics is crucial to cell function and survival. The present study aimed to assess the effects of melatonin on mitochondrial dynamics, TNT formation, and mitochondria transfer in HT22 cells exposed to oxygen/glucose deprivation followed by reoxygenation (OGD/R). The results showed that melatonin treatment during the reoxygenation phase reduced mitochondrial reactive oxygen species (ROS) production, improved cell viability, and increased the expression of PGC1α and SIRT3. Melatonin also preserved the expression of the membrane translocase proteins TOM20 and TIM23, and of the matrix protein HSP60, which are involved in mitochondrial biogenesis. Moreover, it promoted mitochondrial fusion and enhanced the expression of MFN2 and OPA1. Remarkably, melatonin also fostered mitochondrial transfer between injured HT22 cells through TNT connections. These results provide new insights into the effect of melatonin on mitochondrial network reshaping and cell survival. Fostering TNTs formation represents a novel mechanism mediating the protective effect of melatonin in ischemia/reperfusion injury.
科研通智能强力驱动
Strongly Powered by AbleSci AI