PDF(Pubmed)
Abstract：
Endometrial polyps (EPs) are benign overgrowths of the endometrial tissue lining the uterus, often causing abnormal bleeding or infertility. This study analyzed gene expression differences between EPs and adjacent endometrial tissue to elucidate intrinsic abnormalities promoting pathological overgrowth. RNA sequencing of 12 pairs of EPs and the surrounding endometrial tissue from infertile women revealed 322 differentially expressed genes. Protein-protein interaction network analysis revealed significant alterations in specific signaling pathways, notably Wnt signaling and vascular smooth muscle regulation, suggesting these pathways play critical roles in the pathophysiology of EPs. Wnt-related genes DKK1 and DKKL1 were upregulated, while GPC3, GREM1, RSPO3, SFRP5, and WNT10B were downregulated. Relevant genes for vascular smooth muscle contraction were nearly all downregulated in EPs, including ACTA2, ACTG2, KCNMB1, KCNMB2, MYL9, PPP1R12B, and TAGLN. Overall, the results indicate fundamental gene expression changes promote EP formation through unrestrained growth signaling and vascular defects. The intrinsic signaling abnormalities likely contribute to clinical symptoms of abnormal uterine bleeding and infertility common in EP patients. This analysis provides molecular insights into abnormal endometrial overgrowth to guide improved diagnostic and therapeutic approaches for this troublesome women\'s health condition. Confirmation of expanded cohorts and further investigations into implicated regulatory relationships are warranted.
摘要：
子宫内膜息肉（EP）是子宫内膜组织的良性过度生长，常导致异常出血或不孕。这项研究分析了EPs和邻近子宫内膜组织之间的基因表达差异，以阐明促进病理性过度生长的内在异常。来自不育妇女的12对EP和周围子宫内膜组织的RNA测序显示322个差异表达基因。蛋白质-蛋白质相互作用网络分析揭示了特定信号通路的显著改变，特别是Wnt信号和血管平滑肌调节，提示这些途径在EP的病理生理学中起关键作用。Wnt相关基因DKK1和DKKL1上调,而GPC3、GREM1、RSPO3、SFRP5和WNT10B下调。血管平滑肌收缩的相关基因在EP中几乎全部下调，包括ACTA2，ACTG2，KCNMB1，KCNMB2，MYL9，PPP1R12B，还有Tagln.总的来说,结果表明，基本的基因表达变化通过无限制的生长信号和血管缺陷促进EP的形成。内在信号异常可能导致EP患者常见的异常子宫出血和不孕症的临床症状。该分析提供了对异常子宫内膜过度生长的分子见解，以指导这种麻烦的女性健康状况的改进诊断和治疗方法。有必要确认扩大的队列并进一步调查所涉及的监管关系。
