Yang Yuan, Xie Yi, Wu Mengyun, Geng Yanqing, Li Rong, Xu Lei, Liu Xueqing, Pan Yongquan
Laboratory of Reproductive Biology, School of Public Health, Chongqing Medical University, Chongqing 400016, P.R. China.
Department of Obstetrics and Gynecology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.
Mol Med Rep. 2017 Apr;15(4):1547-1554. doi: 10.3892/mmr.2017.6212. Epub 2017 Feb 17.
Decidualization of endometrial stromal cells is an important feature of implantation and pregnancy. The molecular mechanism underlying decidualization remains unclear, particularly regarding the microRNA (miRNA/miR) regulation of this process. The present study revealed the temporal and spatial distribution of mmu‑miR‑96 in the mouse uterus during early pregnancy by reverse transcription‑quantitative polymerase chain reaction and in situ hybridization. In addition, primary stromal cells were isolated from the mouse uterus and used to explore the role of mmu‑miR‑96 in decidualization. The results demonstrated that mmu‑miR‑96 was highly expressed in stromal cells during pregnancy, and was upregulated at implantation sites. In addition, mmu‑miR‑96 was strongly expressed during decidualization, which indicates that it may serve a role in the decidualization of stromal cells. Based on existing reports, mmu‑miR‑96 participates in apoptosis; therefore the present study investigated its effects on the apoptosis of primary endometrial stromal cells. The results indicated that overexpression of mmu‑miR‑96 may induce apoptosis of stromal cells. In further studies regarding the underlying mechanism, the target genes of mmu‑miR‑96 were screened by bioinformatics analysis, and it was confirmed that B‑cell lymphoma 2, an anti‑apoptotic gene, was the target of mmu‑miR‑96, as determined using a reporter gene assay. In conclusion, the present study suggested that mmu‑miR‑96 participates in the decidualization of endometrial stromal cells in mice, thereby serving a key role in pregnancy.
子宫内膜基质细胞的蜕膜化是着床和妊娠的一个重要特征。蜕膜化的分子机制仍不清楚，尤其是关于微小RNA（miRNA/miR）对这一过程的调控。本研究通过逆转录-定量聚合酶链反应和原位杂交揭示了妊娠早期小鼠子宫中mmu-miR-96的时空分布。此外，从小鼠子宫中分离出原代基质细胞，用于探究mmu-miR-96在蜕膜化中的作用。结果表明，mmu-miR-96在妊娠期间的基质细胞中高表达，在着床部位上调。此外，mmu-miR-96在蜕膜化过程中强烈表达，这表明它可能在基质细胞的蜕膜化中发挥作用。基于现有报道，mmu-miR-96参与细胞凋亡；因此，本研究调查了其对原代子宫内膜基质细胞凋亡的影响。结果表明，mmu-miR-96的过表达可能诱导基质细胞凋亡。在关于潜在机制的进一步研究中，通过生物信息学分析筛选出mmu-miR-96的靶基因，并通过报告基因测定法证实抗凋亡基因B细胞淋巴瘤2是mmu-miR-96的靶标。总之，本研究表明mmu-miR-96参与小鼠子宫内膜基质细胞的蜕膜化，从而在妊娠中起关键作用。
