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运动诱导的循环外泌体在临床实践中可能通过抑制平滑肌细胞凋亡来预防盆腔器官脱垂。

Exercise-induced circulating exosomes potentially prevent pelvic organ prolapse in clinical practice via inhibition of smooth muscle apoptosis.

作者信息

Li Yan, Kong Min, Wang Jing, Han Panpan, Zhang Nan, Yang Xin, Wang Juanjuan, Hu Yanling, Duo Yinli, Liu Dan

机构信息

General Hospital of Ningxia Medical University, Ning Xia, China.

Ningxia Medical University, Ning Xia, China.

出版信息

Heliyon. 2022 Dec 25;9(3):e12583. doi: 10.1016/j.heliyon.2022.e12583. eCollection 2023 Mar.

DOI:10.1016/j.heliyon.2022.e12583
PMID:37077375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10106923/
Abstract

BACKGROUND

This study aimed to explore the potential mechanisms of exercise to prevent pelvic organ prolapse (POP) and search for diagnostic indictors for POP.

METHODS

We used two clinical POP datasets with patients' information (GSE12852 and GSE53868), a dataset consisting of altered microRNA expression in circulating blood after exercise (GSE69717) for bioinformatic analysis and clinical diagnostic analysis, while a series of cellular experiments were conducted for preliminary mechanical validation.

RESULTS

Our results show that is highly expressed in the smooth muscle of the ovary and is a key pathogenic gene in POP, while miR-133b is a key molecule in the regulation of POP by exercise-induced serum exosomes. The AUCs of for POP diagnosis were 0.842 and 0.840 in GSE12852 and GSE53868 respectively. At cut-off value = 9.627, the sensitivity and specificity of for predicating POP is 1.000 and 0.833 respectively for GSE53868, while at cut-off value = 3324.640, the sensitivity and specificity of for predicating POP is 0.941 and 0.812 separately for GSE12852. Analysis and experiments confirmed that miR-133b can directly regulate . miR-133b mediated C2C12 myoblasts proliferation and inhibited hydrogen peroxide-induced apoptosis.

CONCLUSIONS

Our study proved that is a good clinical diagnostic indicator for POP and provided a theoretical basis for future prevention of POP through exercise and a potential target for intervention in muscle dysfunction.

摘要

背景

本研究旨在探讨运动预防盆腔器官脱垂(POP)的潜在机制,并寻找POP的诊断指标。

方法

我们使用了两个包含患者信息的临床POP数据集(GSE12852和GSE53868),以及一个由运动后循环血液中微小RNA表达改变组成的数据集(GSE69717)进行生物信息学分析和临床诊断分析,同时进行了一系列细胞实验进行初步的机制验证。

结果

我们的结果表明,[具体基因名称]在卵巢平滑肌中高表达,是POP的关键致病基因,而miR-133b是运动诱导的血清外泌体调节POP的关键分子。在GSE12852和GSE53868中,[具体基因名称]用于POP诊断的AUC分别为0.842和0.840。在GSE53868中,当截断值=9.627时,[具体基因名称]预测POP的敏感性和特异性分别为1.000和0.833,而在GSE12852中,当截断值=3324.640时,[具体基因名称]预测POP的敏感性和特异性分别为0.941和0.812。分析和实验证实,miR-133b可以直接调节[具体基因名称]。miR-133b介导C2C12成肌细胞增殖并抑制过氧化氢诱导的细胞凋亡。

结论

我们的研究证明,[具体基因名称]是POP的良好临床诊断指标,为未来通过运动预防POP提供了理论基础,并为干预肌肉功能障碍提供了潜在靶点。