Background

Alongside many complications in understanding the etiology of Preeclampsia (PE), several determinants, such as the imbalanced proportion of anti-angiogenic/proangiogenic T-cell subsets, especially CD4⁺ (Th17/Treg), as well as alterations in the expression profile of related cytokines, miRNAs, and transcription factors might have been implicated in PE pathogenesis.

Material and method

After sample collection and preparation, CD4⁺ cells were isolated from PE and non-PE pregnant woman and were cultured. Furthermore, analysis such as flow cytometry, real-time PCR, western blotting, and ELISA were performed to assess determinants related to PE manifestation, including sFlt-1, sEng, STAT-3, RORγt, SMAD-7, Foxp3, IL-17, IL-22, Ets-1, and miRNA-326.

Results

Our results showed that the miRNA-326 expression level increased in CD4⁺ Cells and Th17 in PE patients which downregulated Ets-1 expression that acts as a negative control for Th17 development. Furthermore, we showed that the number and expression level of Th17 s and transcription factor RORγt escalated, respectively. While Treg and its related transcription factor (Foxp3) demonstrated a decrease. Flow cytometry analysis illustrated that the Th17/Treg ratio increased in PE. Additionally, we demonstrated that expression and concentration levels of cytokines (IL-17 and IL22) and anti-angiogenic molecules (sEng and sFlt-1) soared in isolated CD4⁺ cells from PE patients, which could be correlated with PE pathogenicity.

Conclusion

In conclusion, we comprehensively evaluated immunological factors and molecules involved in PE manifestation. Interestingly, the CD4⁺ T-cell subset could be an extra source of antiangiogenic factors for the maintenance of this hypertension disorder.

中文翻译：

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一种解决先兆子痫难题的新方法；CD4+ 淋巴细胞中的 MicroRNA-326 可能是一个潜在的嫌疑人

背景

除了在理解先兆子痫 (PE) 的病因方面存在许多并发症外，还有几个决定因素，例如抗血管生成/促血管生成 T 细胞亚群的比例不平衡，尤其是 CD4 ⁺ (Th17/Treg)，以及相关细胞因子、miRNA 和转录因子可能与 PE 发病机制有关。

材料和方法

样品采集和制备后，从PE和非PE孕妇中分离CD4 ⁺细胞并进行培养。此外，还进行了流式细胞术、实时 PCR、蛋白质印迹和 ELISA 等分析以评估与 PE 表现相关的决定因素，包括 sFlt-1、sEng、STAT-3、RORγt、SMAD-7、Foxp3、IL-17 、IL-22、Ets-1 和miRNA-326。

结果

我们的结果表明，在 PE 患者的CD4 ⁺细胞和 Th17 中miRNA-326表达水平增加，这会下调作为 Th17 发展的阴性对照的Ets-1表达。此外，我们发现 Th17 s 和转录因子ROR γ t的数量和表达水平分别升高。而 Treg 及其相关转录因子 (Foxp3) 表现出下降。流式细胞术分析表明，PE 中 Th17/Treg 比值增加。此外，我们证明细胞因子（IL-17 和 IL22）和抗血管生成分子（sEng 和 sFlt-1）的表达和浓度水平在分离的 CD4 ⁺ PE 患者的细胞，这可能与 PE 的致病性有关。

结论

总之，我们综合评估了参与 PE 表现的免疫因素和分子。有趣的是，CD4 ⁺ T 细胞亚群可能是维持这种高血压疾病的抗血管生成因子的额外来源。