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Hsa-miR-498-5p serves as a diagnostic biomarker and regulates endothelial dysfunction via PTEN/AKT pathway in
Man Chen1, Fang Zong1, Jingjing Zhang2
1Department of Obstetrics, Cangzhou Central Hospital, Cangzhou, 061000, China.
Insights
Low miR-498 levels in gestational hypertension (GH) patients indicate poor outcomes. This microRNA inhibits PTEN, suggesting it could be a diagnostic biomarker for GH and endothelial dysfunction.
Area of Science:
- Biochemistry
- Genetics
- Obstetrics
Background:
- Gestational hypertension (GH) is a significant contributor to maternal and fetal complications.
- The role of miR-498 in vascular dysfunction and GH pathogenesis is not well understood.
Purpose of the Study:
- To investigate the expression and function of miR-498 in gestational hypertension.
- To explore the underlying molecular mechanisms of miR-498 in GH.
Main Methods:
- Serum samples from 106 GH patients and 82 controls were analyzed for miR-498 expression.
- Dual-luciferase reporter assay confirmed miR-498 targeting of PTEN.
- In vitro studies in HUVECs assessed miR-498's effects on proliferation, migration, and invasion.
Main Results:
- miR-498 was significantly downregulated in GH patients, showing diagnostic potential.
- Lower miR-498 correlated with higher blood pressure and lower birth weight.
- miR-498 directly targets PTEN, enhancing HUVEC function; PTEN overexpression reversed these effects.
Conclusions:
- Downregulated miR-498 exacerbates endothelial dysfunction in GH via PTEN/AKT inhibition.
- Circulating miR-498 serves as a potential non-invasive biomarker for GH.
- A vascular-specific regulatory axis involving miR-498 and PTEN in GH was identified.
Background:
Gestational hypertension (GH) remains a major cause of maternal and fetal morbidity. miR-498 has been implicated in vascular dysfunction, yet its role and mechanism in GH remain unclear.
Methods:
Clinical serum samples from 106 GH patients and 82 healthy pregnant controls were collected to detect circulating miR-498 expression and analyze its correlation with clinical parameters. The dual-luciferase reporter assay was applied to confirm the direct binding between miR-498 and PTEN. All in vitro functional experiments, including CCK-8 proliferation assay, Transwell migration and invasion assays, were conducted exclusively in HUVECs.
Results:
Hsa-miR-498-5p (miR-498) was significantly downregulated in serum of GH patients and presented favorable diagnostic performance. Circulating miR-498 levels were negatively correlated with systolic blood pressure and neonatal birth weight, while positively correlated with gestational age. Mechanistically, miR-498 directly targeted PTEN. miR-498 overexpression enhanced the proliferative, migratory and invasive capacities of HUVECs, and ectopic PTEN overexpression could reverse these cellular phenotypes.
Conclusion:
Downregulated miR-498 aggravates endothelial dysfunction and facilitates GH progression via inhibiting PTEN/AKT signaling. This study identifies circulating miR-498 as a promising non-invasive diagnostic biomarker and reveals a vascular-specific regulatory axis for GH.
