Yu Ming, Wang Yichun, Cai Jinxuan, Dong Xinyue, Wang Hao, Sun Zichen, Xiao Tianxia, Chen Jie, Li Mengxia, Shan Chunhua, Dong Yang, Zhang Jian V
Center for Energy Metabolism and Reproduction, Shenzhen Key Laboratory of Metabolic Health, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Department of Medical Oncology, The Fourth Hospital of China Medical University, Shenyang, Liaoning, China.
J Cell Mol Med. 2025 Mar;29(6):e70417. doi: 10.1111/jcmm.70417.
Endometrium, the lining of the uterus, changes dynamically in response to fluctuations in ovarian hormones. The proper endocrine environment regulates endometrial functions: menstruation and supporting pregnancy. Obesity is closely related to endometrial dysfunction, which seriously affects women's health and fertility, but the pathological mechanism is unknown. Chemerin is an adipokine involved in multiple biological events such as immunity and metabolism by acting on its functional receptors. This study aimed to characterise the effects of chemerin on human endometrial epithelial cells by RNA-Seq. 12Z cells were utilised as the model because immunoblot results showed that they expressed endometrial markers, epithelial markers and functional receptors for chemerin. Principal component analysis (PCA) showed that chemerin treatment significantly altered the transcriptome. Differential Expression Analysis found 388 significant differentially expressed genes (DEG) in the chemerin treatment group compared with the controls. Gene Set Enrichment Analysis (GSEA) showed that chemerin inhibited lipid metabolism and induced the epithelial-mesenchymal transition (EMT)-like process and cellular senescence. More importantly, GSEA and immunoblots showed that chemerin restrained the STAT3 signalling pathway, which is required for endometrial receptivity establishment. Collectively, these findings provide new evidence that over-produced chemerin underlying the endometrial dysfunctions in obesity.
子宫内膜,即子宫的内膜层,会随着卵巢激素的波动而动态变化。适当的内分泌环境调节着子宫内膜的功能:月经和支持妊娠。肥胖与子宫内膜功能障碍密切相关,这严重影响女性的健康和生育能力,但其病理机制尚不清楚。趋化素是一种脂肪因子,通过作用于其功能性受体参与免疫和代谢等多种生物学事件。本研究旨在通过RNA测序来表征趋化素对人子宫内膜上皮细胞的影响。选用12Z细胞作为模型,因为免疫印迹结果显示它们表达子宫内膜标志物、上皮标志物和趋化素的功能性受体。主成分分析(PCA)表明,趋化素处理显著改变了转录组。差异表达分析发现,与对照组相比,趋化素处理组有388个显著差异表达基因(DEG)。基因集富集分析(GSEA)表明,趋化素抑制脂质代谢并诱导类似上皮-间质转化(EMT)的过程和细胞衰老。更重要的是,GSEA和免疫印迹表明,趋化素抑制了子宫内膜容受性建立所需的STAT3信号通路。总的来说,这些发现提供了新的证据,表明肥胖中过量产生的趋化素是子宫内膜功能障碍的潜在原因。