Study on the Expression of MiR-642b-3p in Spontaneous Intracerebral Hemorrhage and Its Regulatory Mechanism on Endothelial Cell Injury.

Spontaneous cerebral hemorrhage (sICH) is one of the cerebrovascular diseases with the highest mortality rate. MicroRNAs (miRNAs) are implicated in the regulation of various pathological processes, however, the specific function of miR-642b-3p in sICH remains unclear. Serum miR-642b-3p levels of sICH patients was determined. A thrombin-induced human brain microvascular endothelial cell (hBMECs) injury model was established. Cell viability, apoptosis, inflammatory factors, and related protein expression were assessed using CCK-8 assay, flow cytometry, ELISA, and Western blot. The targeting relationship between miR-642b-3p and CCNA2 was validated via a dual-luciferase reporter assay. MiR-642b-3p in the serum of ICH patients was significantly increased. Following thrombin induction, miR-642b-3p was upregulated in hBMECs, accompanied by decreased cell viability, increased apoptosis, elevated production of inflammatory factors, upregulated expression of pro-apoptotic proteins (Bax and cleaved caspase-3), and downregulated expression of anti-apoptotic protein (Bcl-2). Additionally, the protein levels of tight junction markers ZO-1 and occludin were markedly decreased. Notably, inhibition of miR-642b-3p significantly reversed these thrombin-induced changes and alleviated cell damage. Mechanistically, CCNA2was confirmed as a direct downstream target gene of miR-642b-3p. MiR-642b-3p is upregulated in sICH and mediates thrombin-induced endothelial cell injury, at least in part, by targeting CCNA2. These findings suggest that the miR-642b-3p/CCNA2 axis may represent a potential mechanistic pathway involved in ICH-induced blood-brain barrier disruption.