miR-205-3p inhibits porphyromonas gingivalis lipopolysaccharide-induced human umbilical vein endothelial cells inflammation and apoptosis by targeting PRMT5

Objective

This study aimed to investigate the regulatory mechanism of miR-205–3p in Porphyromonas gingivalis lipopolysaccharide (P.g-LPS)-induced atherosclerosis.

Design

In an in vitro setting, human umbilical vein endothelial cells (HUVECs) were exposed to P.g-LPS to simulate the vascular endothelial damage induced by periodontitis. Subsequently, ELISA and flow cytometry were employed to assess the inflammatory response and apoptotic status of these cells.To quantify the expression levels of protein arginine methyltransferase 5 (PRMT5), BCL2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), P65 and miR-205–3p within the HUVECs, Western Blot and qPCR were respectively utilized. Moreover, small interfering RNA (siRNA) targeting PRMT5 and miR-205–3p were applied to monitor the changes in PRMT5 expression. Bioinformatics analysis was carried out to predict the potential binding sites between miR-205–3p and PRMT5. Finally, the interaction between miR-205–3p and PRMT5 was validated through the dual-luciferase reporter assay.

Results

The results indicate that P.g-LPS intervention exacerbates damage to HUVECs and increases the expression of PRMT5. Silencing PRMT5 reduces cell inflammation and apoptosis. After stimulation with P.g-LPS, the level of miR-205–3p decreases, and its overexpression alleviates inflammation and apoptosis in the cells. Bioinformatics analysis and dual luciferase reporter assays confirm that PRMT5 is a target of miR-205–3p, and the overexpression of PRMT5 can reverse the protective effects of miR-205–3p.

Conclusion

miR-205–3p can mitigate vascular endothelial injury by decreasing PRMT5 expression, providing new insights for potential treatments.