Department of Obstetrics and Gynaecology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China; The Second School of Medicine, Wenzhou Medical University, Zhejiang 325000, Wenzhou, China.
Department of Obstetrics and Gynaecology, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325000, China.
Int Immunopharmacol. 2023 Apr;117:109644. doi: 10.1016/j.intimp.2022.109644. Epub 2023 Mar 4.
To investigate the roles of the cGAS-STING signal pathway and autophagy in the disease progression of endometriosis and to explore the regulatory mechanism of the cGAS-STING signal pathway on autophagy.
A case-control experimental study, in vitro primary cell culture study, and in vivo animal research.
Immunohistochemistry, RT-PCR and Western Blot were used to detect cGAS-STING signal pathway and autophagy expression differences in human and rat models. The lentivirus was used to overexpress STING in cells. The expression level of autophagy in human endometrial stromal cells (HESCs) transfected with lv-STING was detected by Western Blot, RT-PCR, and immunofluorescence. Transwell migration and invasion assays were conducted to assess cellular motility. The STING antagonist was applicated in vivo to investigate the therapeutic effects.
The expression levels of the cGAS-STING signal pathway and autophagy in Human and Rat ectopic endometrium were increased. STING overexpression promotes the expression of autophagy in human endometrial stromal cells (HESCs). STING overexpression enhances the migration and invasion of the human endometrial stromal cells (HESCs), but the addition of autophagy antagonists could significantly reverse this. STING antagonists inhibited the expression of autophagy in vivo and reduced the volume of ectopic lesions.
The expression levels of the cGAS-STING signal pathway and autophagy were increased in endometriosis. cGAS-STING signal pathway promotes the development of endometriosis by upregulating autophagy.
探讨 cGAS-STING 信号通路和自噬在子宫内膜异位症疾病进展中的作用，并探索 cGAS-STING 信号通路对自噬的调控机制。
病例对照实验研究、体外原代细胞培养研究和体内动物研究。
免疫组织化学、RT-PCR 和 Western blot 用于检测人及大鼠模型中 cGAS-STING 信号通路和自噬表达差异。慢病毒转染过表达 STING。Western blot、RT-PCR 和免疫荧光检测转染 lv-STING 的人子宫内膜基质细胞（HESCs）中自噬的表达水平。Transwell 迁移和侵袭实验评估细胞迁移能力。体内应用 STING 拮抗剂探讨治疗效果。
人及大鼠异位内膜中 cGAS-STING 信号通路和自噬的表达水平升高。STING 过表达促进人子宫内膜基质细胞（HESCs）中自噬的表达。STING 过表达增强人子宫内膜基质细胞（HESCs）的迁移和侵袭能力，但自噬拮抗剂的添加可显著逆转这一作用。STING 拮抗剂体内抑制自噬的表达并减少异位病灶的体积。
子宫内膜异位症中 cGAS-STING 信号通路和自噬的表达水平升高。cGAS-STING 信号通路通过上调自噬促进子宫内膜异位症的发展。
