Background. Gestational diabetes mellitus (GDM) seriously affects the health of mothers and infants. The high-glucose-induced inhibition in trophoblast cell viability is an important event in GDM pathogenesis. This study evaluated the expression and clinical significance of miR-136 in GDM patients, and the biological function and related mechanisms of miR-136 in the regulation of trophoblast cell proliferation were explored. Methods. The expression of miR-136 in serum and placenta of GDM patients was measured using quantitative Real-Time PCR. Trophoblast cells were stimulated with high-glucose medium to mimic the pathological changes of GDM, and the effect of miR-136 was examined by CCK-8 assay. A luciferase reporter assay was used to confirm the target gene of miR-136, and the relationship of E2F transcription factor 1 (E2F1) with miR-136 in GDM was further analyzed. Results. miR-136 expression was significantly elevated in GDM serum and tissue samples. By high-glucose treatment, trophoblast cell proliferation was inhibited and miR-136 expression was promoted. The knockdown of miR-136 could promote the proliferation of trophoblast cells exposed to high glucose, whereas the overexpression of miR-136 could suppress it. In addition, E2F1 was identified as a target gene of miR-136, which could mediate the regulatory effect of miR-136 on trophoblast cell proliferation. Conclusion. Collectively, miR-136 expression is increased in both serum and placental tissues in GDM patients, and miR-136 mediates the inhibiting effect of high glucose on trophoblast cell viability by targeting E2F1.

中文翻译：

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miR-136在妊娠期糖尿病中的差异表达通过靶向E2F1介导高糖诱导的滋养层细胞损伤

背景。妊娠期糖尿病（GDM）严重影响母婴健康。高糖诱导的滋养层细胞活力抑制是 GDM 发病机制中的一个重要事件。本研究评估了miR-136在GDM患者中的表达及临床意义，探讨了miR-136在调节滋养层细胞增殖中的生物学功能及相关机制。方法. 使用定量实时 PCR 测量 GDM 患者血清和胎盘中 miR-136 的表达。用高糖培养基刺激滋养层细胞以模拟GDM的病理变化，并通过CCK-8法检测miR-136的作用。荧光素酶报告基因检测用于确认miR-136的靶基因，并进一步分析GDM中E2F转录因子1（E2F1）与miR-136的关系。结果. GDM 血清和组织样本中 miR-136 的表达显着升高。通过高糖处理，滋养层细胞增殖受到抑制，miR-136表达得到促进。miR-136的敲低可以促进暴露于高葡萄糖的滋养层细胞的增殖，而miR-136的过表达可以抑制它。此外，E2F1被鉴定为miR-136的靶基因，可介导miR-136对滋养层细胞增殖的调节作用。结论。总的来说，GDM 患者血清和胎盘组织中 miR-136 的表达均增加，miR-136 通过靶向 E2F1 介导高糖对滋养层细胞活力的抑制作用。