Department of Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Zhejiang, 310006, China.
Department of Gynecology, Women's Hospital, School of Medicine, Zhejiang University, Zhejiang, 310006, China.
Free Radic Biol Med. 2019 May 20;136:22-34. doi: 10.1016/j.freeradbiomed.2019.03.027. Epub 2019 Mar 27.
Endometriosis is associated with inflammatory reaction, and reactive oxidative species (ROS) are highly pro-inflammatory factors. Mitochondria are responsible for the production of ROS and energy. However, little is known about how mitochondria regulate ROS generation and energy metabolism in endometriosis. In our study, we investigated mitochondrial structure and function of ectopic endometrial stromal cells (ESCs) in ovarian endometriosis. We found mitochondria in ectopic ESCs generated more ROS and energy than controlled groups. Mitochondrial superoxide dismutase (SOD2), as an antioxidant enzyme, was found highly expressed in ectopic endometrium compared with normal endometrium. Due to its antioxidant role, SOD2 promoted the development of endometriosis by maintaining functional mitochondria to support high energetic metabolism of ectopic ESCs. We also showed that SOD2 promoted cell proliferation and migration in ovarian endometriosis. Inhibiting SOD2 expression reduced proliferation and migration of ectopic ESCS, and increased cell apoptosis. Therefore, understanding the role of mitochondrial dysfunction and SOD2 in ovarian endometriosis may provide new strategies to treat this disease.
子宫内膜异位症与炎症反应有关，而活性氧（ROS）是高度促炎的因素。线粒体负责 ROS 的产生和能量代谢。然而，对于线粒体如何调节子宫内膜异位症中 ROS 的产生和能量代谢知之甚少。在我们的研究中，我们研究了卵巢子宫内膜异位症中异位子宫内膜基质细胞（ESC）的线粒体结构和功能。我们发现异位 ESC 中的线粒体产生的 ROS 和能量比对照组多。线粒体超氧化物歧化酶（SOD2）作为一种抗氧化酶，在异位子宫内膜中表达高于正常子宫内膜。由于其抗氧化作用，SOD2 通过维持功能线粒体来支持异位 ESC 的高能量代谢，从而促进子宫内膜异位症的发展。我们还表明，SOD2 促进卵巢子宫内膜异位症中的细胞增殖和迁移。抑制 SOD2 的表达减少了异位 ESC 的增殖和迁移，并增加了细胞凋亡。因此，了解线粒体功能障碍和 SOD2 在卵巢子宫内膜异位症中的作用可能为治疗这种疾病提供新的策略。
