Endometrial stromal cell MiR-29c-3p microRNA regulates uterine contraction.
Endometrial stromal cell MiR-29c-3p microRNA regulates uterine contraction.
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子宫内膜基质细胞 MiR-29c-3p microRNA 调节子宫收缩。
DOI：
10.1530/rep-19-0196
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发表时间：
2019-12
期刊：
影响因子：
3.8
通讯作者：
Li Yanping
中科院分区：
文献类型：
--
作者：
Xiao Lan;Zhang Qiong;Huang Xi;He Aihua;Xie Shi;Li Yanping
子宫蠕动在生育和女性生殖健康中起着至关重要的作用。虽然子宫蠕动被认为与某些激素和子宫病理有关，但其生理机制尚不清楚。本研究旨在检测异常高频（高）和低频（低）蠕动患者子宫内膜中microRNA （miRNA）的变化，以阐明miRNA是否调节子宫蠕动。我们使用miRNA微阵列和RT-qPCR来鉴定子宫内膜组织中miRNA的变化，在共培养的人子宫内膜基质细胞（ESCs）上使用胶原凝胶收缩实验来分析miRNA调节的改变如何影响子宫平滑肌（USM）收缩，并使用western blots和其他实验来阐明潜在的机制。我们发现，在几种差异调节的mirna中，miR-29c-3p在低蠕动患者的子宫内膜样本中过表达；垂体后叶催产素受体（OXTR）在垂体功能亢进患者的子宫内膜样本中表达较低。生物信息学分析和荧光素酶测定表明，OXTR是miR-29c-3p的靶标，从而减弱其表达。此外，ESC培养物中miR-29c-3p的下调增加了醛酮还原酶家族1成员C3 （AKR1C3）的表达，并增加了前列腺素F2α (PGF2α)的释放。共培养过表达miR-29c-3p的ESCs减少USM细胞收缩；当转染miR-29c-3p抑制剂时，发现相反的趋势。综上所述，子宫内膜细胞中的miR-29c-3p通过减弱OXTR的表达和减少PGF2α的释放来调节子宫收缩性。
Uterine peristalsis plays a vital role in fertility and female reproductive health. Although uterine peristalsis is thought to be correlated with some hormones and uterine pathologies, the physiological mechanisms underlying uterine peristalsis remain not quite clear. This study aimed to identify changes in microRNA (miRNA) in the endometrium of patients with abnormally high-frequency (hyper-) and low-frequency (hypo-) peristalsis to clarify whether miRNAs regulate uterine peristalsis. We used a miRNA microarray and RT-qPCR to identify changes in miRNA in endometrial tissue, a collagen gel contraction assay on co-cultured human endometrial stromal cells (ESCs) to analyze how the altered regulation of miRNAs influences uterine smooth muscle (USM) contraction, and western blots and other assays to elucidate the potential mechanisms involved. We found that among several differentially-regulated miRNAs, miR-29c-3p was overexpressed in endometrial samples from patients with hypoperistalsis; oxytocin receptor (OXTR) expression was low in endometrial samples from patients with hypoperistalsis. Bioinformatic analysis and luciferase assays indicated that OXTR is a target of miR-29c-3p, which attenuates its expression. Additionally, downregulation of miR-29c-3p in ESC cultures increased the expression of aldo-keto reductase family 1, member C3 (AKR1C3) and increased release of prostaglandin F2 alpha (PGF2α). Co-cultured ESCs overexpressing miR-29c-3p reduced USM cell contractions; the opposite tendency was found when ESCs were transfected with a miR-29c-3p inhibitor. To conclude, miR-29c-3p in endometrial cells regulates uterine contractility by attenuating expression of OXTR and reducing PGF2α release.
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