Hypertension in pregnancy · 2026
MIR210HG promotes preeclampsia progression through CDHR5.
СтатьяНазвание и аннотация: Перевод в очереди
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Sun Ningxia, Zhang Lu, Xu Jine, Han Mengmeng, Chen Aiping, Liu Shiguo
Аннотация
OBJECTIVE: Early diagnosis of preeclampsia (PE) remains challenging. We previously linked the long non-coding (lnc) RNA MIR210HG to pathological placental development. Here, we investigated its differential expression, pathophysiological phenotypic specificity, and non-invasive diagnostic potential for PE in the peripheral blood and placental tissue.
METHODS: We enrolled 88 PE patients (case group) and 81 normal pregnant women (control group) from the Affiliated Hospital of Qingdao University during January 2020-December 2021. MIR210HG expression was detected via RT-PCR and western blotting, and was modulated using siRNA/overexpression plasmid transfection in human trophoblasts and vascular endothelial cells.
RESULTS: MIR210HG expression was specifically upregulated in the peripheral blood of patients with early-onset PE, with superior diagnostic efficacy for the PE-fetal growth restriction subtype. Additionally, CDHR5 was upregulated in PE-associated placental tissues (P = 0.004). Cellular assays confirmed that MIR210HG knockdown reduced CDHR5 expression in trophoblasts and endothelial cells (Bewo: P = 0.019; JEG3: P = 0.006), and CDHR5 knockdown also downregulated MIR210HG expression (Bewo: P = 0.023).
CONCLUSION: Therefore, MIR210HG may contribute to placental pathological injury by regulating CDHR5, though the pathogenic mechanism remains unclear. In contrast to the invasive and lagging placental-derived lncRNA biomarkers reported in previous studies, peripheral blood MIR210HG allows for non-invasive monitoring during pregnancy, making it more clinically applicable for early screening and phenotypic stratification of PE.
METHODS: We enrolled 88 PE patients (case group) and 81 normal pregnant women (control group) from the Affiliated Hospital of Qingdao University during January 2020-December 2021. MIR210HG expression was detected via RT-PCR and western blotting, and was modulated using siRNA/overexpression plasmid transfection in human trophoblasts and vascular endothelial cells.
RESULTS: MIR210HG expression was specifically upregulated in the peripheral blood of patients with early-onset PE, with superior diagnostic efficacy for the PE-fetal growth restriction subtype. Additionally, CDHR5 was upregulated in PE-associated placental tissues (P = 0.004). Cellular assays confirmed that MIR210HG knockdown reduced CDHR5 expression in trophoblasts and endothelial cells (Bewo: P = 0.019; JEG3: P = 0.006), and CDHR5 knockdown also downregulated MIR210HG expression (Bewo: P = 0.023).
CONCLUSION: Therefore, MIR210HG may contribute to placental pathological injury by regulating CDHR5, though the pathogenic mechanism remains unclear. In contrast to the invasive and lagging placental-derived lncRNA biomarkers reported in previous studies, peripheral blood MIR210HG allows for non-invasive monitoring during pregnancy, making it more clinically applicable for early screening and phenotypic stratification of PE.