MIR210HG promotes preeclampsia progression through CDHR5

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.

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.

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).

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.