Pelvic organ prolapse (POP) is a common disorder among women that negatively affects women’s quality of life. Early growth response 2 (EGR2) is a transcription factor that regulates cell growth. The present study aimed to explore the role of EGR2 in POP progression and provided a new target for the treatment and prevention of POP. Firstly, we extracted primary vaginal anterior wall fibroblasts from POP tissues and non-POP tissues and then constructed an EGR2-silencing lentivirus for further study. Immunoblotting, qPCR, TUNEL assay, CCK-8 assay, dual luciferase assay, and ELISA assay were carried out. EGR2 expression was much higher in POP tissues than in control tissues, and EGR2 expression positively correlated with cytokine signaling 3 (SOCS3) expression. Knockdown of EGR2 increased cell proliferation, upregulated PCNA expression, and reduced apoptosis in POP fibroblasts. Moreover, we found that the knockdown of EGR2 increased COL1A1, COL3A1, and Elastin expression and decreased MMP2 and MMP9 activities, and knockdown of EGR2 increased TGF-β/Smad pathway activity in POP fibroblasts. Interestingly, the results of dual luciferase assay demonstrated that EGR2 was able to increase SOCS3 transcriptional activity. EGR2 knockdown alleviated the apoptosis of POP fibroblasts by reducing SOCS3 expression and improving the proliferation and collagen synthesis of POP fibroblasts. Overall, our study illustrated that EGR2 was highly expressed in POP tissues, and knockdown of EGR2 alleviated apoptosis and reduced matrix degradation in POP fibroblasts. This study might provide a new insight into the pathogenesis of POP.

盆腔器官脱垂（POP）是女性常见的疾病，对女性的生活质量产生负面影响。早期生长反应 2 (EGR2) 是一种调节细胞生长的转录因子。本研究旨在探讨EGR2在POP进展中的作用，为POP的治疗和预防提供新的靶点。首先，我们从POP组织和非POP组织中提取原代阴道前壁成纤维细胞，然后构建EGR2沉默慢病毒以供进一步研究。进行了免疫印迹、qPCR、TUNEL 测定、CCK-8 测定、双荧光素酶测定和 ELISA 测定。 POP组织中EGR2的表达量远高于对照组织，且EGR2的表达量与细胞因子信号传导3（SOCS3）的表达量呈正相关。 EGR2 的敲除增加了 POP 成纤维细胞的细胞增殖、上调 PCNA 表达并减少细胞凋亡。此外，我们发现EGR2的敲低增加了POP成纤维细胞中COL1A1、COL3A1和弹性蛋白的表达并降低了MMP2和MMP9的活性，并且EGR2的敲低增加了POP成纤维细胞中的TGF-β/Smad通路活性。有趣的是，双荧光素酶测定的结果表明EGR2能够增加SOCS3转录活性。 EGR2敲低通过减少SOCS3表达并改善POP成纤维细胞的增殖和胶原合成来减轻POP成纤维细胞的凋亡。总体而言，我们的研究表明 EGR2 在 POP 组织中高表达，EGR2 的敲低可减轻 POP 成纤维细胞的细胞凋亡并减少基质降解。这项研究可能为 POP 的发病机制提供新的见解。