Graduate School, Dalian Medical University, Liaoning, People's Republic of China.
Reproduction Medicine Centre, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, People's Republic of China.
Redox Rep. 2024 Dec;29(1):2377870. doi: 10.1080/13510002.2024.2377870. Epub 2024 Jul 15.
To observe the CISD2 expression among PCOS patients and to explore its profound impact on the follicular microenvironment. Moreover, we want to elucidate the intricate mechanistic contribution of to the onset and progression of PCOS.
Oxidase NOX2, mitophagy-related proteins, and CISD2 were detected by WB. The changes in mitochondrial structure and quantity were observed by transmission electron microscopy. Mitochondrial and lysosome colocalization was used to detect the changes of mitophagy. MDA kit, GSH and GSSG Assay kit and ROS probe were used to detect oxidative stress damage.
We found that CISD2, mitophagy and oxidase in the GCs of PCOS patients were significantly increased. Testosterone stimulation leads to the increase of oxidase, mitophagy, and CISD2 in KGN cells. inhibition promoted the increase of mitophagy, and the activation of mitochondria-lysosome binding, while alleviating the oxidative stress.
Inhibition of CISD2 can improve the occurrence of oxidative stress by increasing the level of mitophagy, thus affecting the occurrence and development of PCOS diseases.
观察多囊卵巢综合征(PCOS)患者中 CISD2 的表达,探讨其对卵泡微环境的深远影响。此外,我们希望阐明 CISD2 对 PCOS 发病和进展的复杂作用机制。
通过 WB 检测氧化酶 NOX2、线粒体自噬相关蛋白和 CISD2。通过透射电子显微镜观察线粒体结构和数量的变化。线粒体和溶酶体共定位检测自噬的变化。MDA 试剂盒、GSH 和 GSSG 测定试剂盒和 ROS 探针用于检测氧化应激损伤。
我们发现 PCOS 患者的 GC 中 CISD2、线粒体自噬和氧化酶明显增加。睾酮刺激导致 KGN 细胞中氧化酶、线粒体自噬和 CISD2 的增加。抑制 CISD2 可促进线粒体-溶酶体结合的增加和自噬,同时减轻氧化应激。
抑制 CISD2 可通过增加线粒体自噬水平来改善氧化应激的发生,从而影响 PCOS 疾病的发生和发展。