Hao Zhang, Xinlu Wang, Meng Dong, Jie Wang, Weidong Ren
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Results revealed an up-regulation of miR-5195-3p expression in these tissues, showing a negative correlation with the expression of extracellular matrix-related proteins. Further analysis using bioinformatics tools identified Lipoxygenase (LOX) as a potential target in pelvic organ prolapse. Dual luciferase reporter gene experiments confirmed LOX as a direct target of miR-5195-3p. Interestingly, regulating the expression of LOX also influenced the transforming growth factor β1 signaling pathway and had an impact on extracellular matrix metabolism. This finding suggests that miR-5195-3p controls extracellular matrix metabolism by targeting LOX and modulating the TGF-β1 signaling pathway. In conclusion, this study unveils the involvement of miR-5195-3p in the pathological mechanism of pelvic organ prolapse by regulating extracellular matrix metabolism through the LOX/TGF-β1 axis. These findings reveal new mechanisms in the pathogenesis of pelvic organ prolapse, providing a theoretical foundation and therapeutic targets for further research on pelvic organ prolapse treatment.</p>","PeriodicalId":8965,"journal":{"name":"Biology of Reproduction","volume":" ","pages":"86-101"},"PeriodicalIF":3.1000,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Unveiling novel regulatory mechanisms of miR-5195-3p in pelvic organ prolapse pathogenesis†.\",\"authors\":\"Hao Zhang, Xinlu Wang, Meng Dong, Jie Wang, Weidong Ren\",\"doi\":\"10.1093/biolre/ioae162\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Pelvic organ prolapse is a condition that significantly affects women's quality of life. The pathological mechanism of pelvic organ prolapse is not yet fully understood, and its pathogenesis is often caused by multiple factors, including the metabolic imbalance of the extracellular matrix. This study aims to investigate the role of miR-5195-3p, a microRNA, in the pathology of pelvic organ prolapse and its regulatory mechanism. Using various molecular biology techniques such as real-time reverse transcription Polymerase Chain Reaction (PCR), fluorescence in situ hybridization, immunohistochemistry, and Western blot, miR-5195-3p expression was examined in vaginal wall tissues obtained from pelvic organ prolapse patients. Results revealed an up-regulation of miR-5195-3p expression in these tissues, showing a negative correlation with the expression of extracellular matrix-related proteins. Further analysis using bioinformatics tools identified Lipoxygenase (LOX) as a potential target in pelvic organ prolapse. Dual luciferase reporter gene experiments confirmed LOX as a direct target of miR-5195-3p. Interestingly, regulating the expression of LOX also influenced the transforming growth factor β1 signaling pathway and had an impact on extracellular matrix metabolism. This finding suggests that miR-5195-3p controls extracellular matrix metabolism by targeting LOX and modulating the TGF-β1 signaling pathway. In conclusion, this study unveils the involvement of miR-5195-3p in the pathological mechanism of pelvic organ prolapse by regulating extracellular matrix metabolism through the LOX/TGF-β1 axis. 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引用次数: 0
摘要
盆腔器官脱垂(POP)是一种严重影响妇女生活质量的疾病。POP 的病理机制尚未完全明了,其发病往往由多种因素引起,包括细胞外基质(ECM)的代谢失衡。本研究旨在探讨微RNA miR-5195-3p在POP病理中的作用及其调控机制。研究采用 qRT-PCR、FISH、免疫组织化学和 Western 印迹等多种分子生物学技术,检测了 POP 患者阴道壁组织中 miR-5195-3p 的表达。结果显示,这些组织中 miR-5195-3p 的表达呈上调趋势,与 ECM 相关蛋白的表达呈负相关。利用生物信息学工具进行的进一步分析发现,LOX 是 POP 的一个潜在靶点。双荧光素酶报告基因实验证实 LOX 是 miR-5195-3p 的直接靶标。有趣的是,调节 LOX 的表达也会影响 TGF-β1 信号通路,并对 ECM 代谢产生影响。这一发现表明,miR-5195-3p 通过靶向 LOX 和调节 TGF-β1 信号通路来控制 ECM 的新陈代谢。总之,本研究揭示了 miR-5195-3p 通过 LOX/TGF-β1 轴调节 ECM 代谢参与 POP 病理机制的过程。这些发现揭示了盆腔 POP 发病的新机制,为进一步研究 POP 治疗提供了理论基础和治疗靶点。
Unveiling novel regulatory mechanisms of miR-5195-3p in pelvic organ prolapse pathogenesis†.
Pelvic organ prolapse is a condition that significantly affects women's quality of life. The pathological mechanism of pelvic organ prolapse is not yet fully understood, and its pathogenesis is often caused by multiple factors, including the metabolic imbalance of the extracellular matrix. This study aims to investigate the role of miR-5195-3p, a microRNA, in the pathology of pelvic organ prolapse and its regulatory mechanism. Using various molecular biology techniques such as real-time reverse transcription Polymerase Chain Reaction (PCR), fluorescence in situ hybridization, immunohistochemistry, and Western blot, miR-5195-3p expression was examined in vaginal wall tissues obtained from pelvic organ prolapse patients. Results revealed an up-regulation of miR-5195-3p expression in these tissues, showing a negative correlation with the expression of extracellular matrix-related proteins. Further analysis using bioinformatics tools identified Lipoxygenase (LOX) as a potential target in pelvic organ prolapse. Dual luciferase reporter gene experiments confirmed LOX as a direct target of miR-5195-3p. Interestingly, regulating the expression of LOX also influenced the transforming growth factor β1 signaling pathway and had an impact on extracellular matrix metabolism. This finding suggests that miR-5195-3p controls extracellular matrix metabolism by targeting LOX and modulating the TGF-β1 signaling pathway. In conclusion, this study unveils the involvement of miR-5195-3p in the pathological mechanism of pelvic organ prolapse by regulating extracellular matrix metabolism through the LOX/TGF-β1 axis. These findings reveal new mechanisms in the pathogenesis of pelvic organ prolapse, providing a theoretical foundation and therapeutic targets for further research on pelvic organ prolapse treatment.
期刊介绍:
Biology of Reproduction (BOR) is the official journal of the Society for the Study of Reproduction and publishes original research on a broad range of topics in the field of reproductive biology, as well as reviews on topics of current importance or controversy. BOR is consistently one of the most highly cited journals publishing original research in the field of reproductive biology.