Activation of ATF3/AP-1 signaling pathway is required for P2X3-induced endometriosis pain

ATF3/AP-1 信号通路的激活是 P2X3 诱发子宫内膜异位症疼痛的必要条件

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作者:Shaojie Ding, Qin Yu, Jianzhang Wang, Libo Zhu, Tiantian Li, Xinyue Guo, Xinmei Zhang

Methods

Degrees of hyperalgesia, endogenous adenosine 5'-triphosphate (ATP) contents and P2X3 expression levels in endometriotic lesions and DRG tissues were detected in a rat model of endometriosis. The expression levels of ATF3 and P2X3 were measured using qRT-PCR, western blot analysis and immunofluorescence analysis after adenosine 5'-diphosphate (ADP) exposure in DRG cells. Plasmids encoding ATF3 and its siRNA were used to investigate the role of ATF3 on ADP-induced P2X3 upregulation. The activity of ATF binding to the P2X3 promoter was evaluated by using chromatin immunoprecipitation (CHIP) and luciferase assays. SP600125, an inhibitor of c-JUN N-terminal kinase, was wrapped in CSOSA/LPs delivery system and its inhibitory effects on ADP-induced upregulation of P2X3 in DRG cells and endometriosis-induced hyperalgesia in rats were tested. Main

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