Xiao Biru, Zhang Wenmiao, Ji Nini, Chen Qiuyue
Department of Obstetrical, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
Department of Obstetrical, The First Affiliated Hospital of Wenzhou Medical University, Nanbaixiang Street, Ouhai District, Wenzhou, Zhejiang, 325000, China.
Open Med (Wars). 2025 Jan 13;20(1):20241119. doi: 10.1515/med-2024-1119. eCollection 2025.
Gestational diabetes mellitus (GDM), defined as glucose intolerance occurring or first detected during pregnancy, affects approximately 8% of pregnancies worldwide. The dysfunction of trophoblasts in pregnancies complicated by GDM is associated with changes in trophoblast cell functions, resulting in compromised proliferation and regulation of the cell cycle. Cyclin B1 (CCNB1), a pivotal controller of the start of mitosis, is crucial in these mechanisms. Nevertheless, the precise function of CCNB1 in trophoblast dysfunction related to GDM has not been extensively investigated. The aim of this study was to investigate CCNB1's role in high glucose (HG)-triggered trophoblast. Herein, we revealed that in HG-stimulated HTR8/SVneo cells, CCNB1 is highly expressed. Knockdown of CCNB1 significantly promotes the growth of HG-stimulated HTR8/SVneo cells and suppresses inflammation ( < 0.05). Additionally, reducing CCNB1 expression significantly improves glucose uptake and inhibits the Wnt/β-catenin pathway in HG-stimulated HTR8/SVneo cells ( < 0.05). In conclusion, our study demonstrated that the deletion of CCNB1 can alleviate trophoblast dysfunction induced by HG in GDM through the Wnt/β-catenin pathway. This suggests that CCNB1 may be a potential target for managing GDM. Although our results underscore the potential therapeutic benefits of reducing CCNB1 in mitigating trophoblast dysfunction, it is important to note that the study is limited by its reliance on a single cell line and the absence of validation.
妊娠期糖尿病（GDM）定义为在孕期发生或首次检测出的葡萄糖不耐受，影响全球约8%的妊娠。患有GDM的妊娠中滋养层细胞功能障碍与滋养层细胞功能变化相关，导致细胞增殖受损和细胞周期调控异常。细胞周期蛋白B1（CCNB1）是有丝分裂开始的关键调控因子，在这些机制中至关重要。然而，CCNB1在与GDM相关的滋养层细胞功能障碍中的具体作用尚未得到广泛研究。本研究的目的是探讨CCNB1在高糖（HG）诱导的滋养层细胞中的作用。在此，我们发现，在HG刺激的HTR8/SVneo细胞中，CCNB1高表达。敲低CCNB1可显著促进HG刺激的HTR8/SVneo细胞生长并抑制炎症（<0.05）。此外，降低CCNB1表达可显著改善HG刺激的HTR8/SVneo细胞的葡萄糖摄取并抑制Wnt/β-连环蛋白信号通路（<0.05）。总之，我们的研究表明，CCNB1的缺失可通过Wnt/β-连环蛋白信号通路减轻GDM中HG诱导的滋养层细胞功能障碍。这表明CCNB1可能是治疗GDM的潜在靶点。尽管我们的结果强调了降低CCNB1在减轻滋养层细胞功能障碍方面的潜在治疗益处，但需要注意的是，该研究受限于仅依赖单一细胞系且缺乏验证。
