miR-1307-5p mediates endothelial dysfunction and inflammation induced by acute coronary syndrome by targeting PIM3.

OBJECTIVE

This study aims to investigate the clinical value of miR-1307-5p in acute coronary syndrome (ACS) patients and its role in human umbilical vein endothelial cells (HUVECs).

METHODS

Enrollment consisted of 124 ACS cases and 124 controls. Reverse transcription quantitative real-time PCR (RT-qPCR) was used to measure the miR-1307-5p and proviral integration site for Moloney murine leukemia virus 3 (PIM3) levels in serum samples, and the receiver operating characteristic (ROC) curve was utilized to assess the diagnostic utility of miR-1307-5p. ACS cell model was established using hypoxia/reoxygenation (H/R). enzyme-linked immunosorbent assay (ELISA) was employed to detect the von Willebrand factor (vWF), heart-type fatty acid-binding protein (H-FABP), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-8 in serum and HUVECs. Apoptosis was analyzed by flow cytometry, while cell viability was evaluated through Cell Counting Kit-8 (CCK8) assay. The interaction between miR-1307-5p and PIM3 was validated via dual-luciferase reporter (DLR) and RNA immunoprecipitation (RIP) experiments.

RESULTS

miR-1307-5p is significantly downregulated in ACS patients' serum and effectively distinguishes controls from ACS patients. It also shows negative correlations with vWF, H-FABP, TNF-α, IL-6, and IL-8. miR-1307-5p directly targets PIM3. Upregulating miR-1307-5p enhances HUVEC viability and suppresses apoptosis. Furthermore, this intervention alleviates endothelial injury and reduces inflammation. Notably, PIM3 overexpression reversed these protective effects of miR-1307-5p.

CONCLUSION

Reduced serum miR-1307-5p expression holds promise as a potential diagnostic biomarker for ACS. Upregulation of miR-1307-5p alleviates endothelial dysfunction and inflammation by targeting PIM3, suggesting that the miR-1307-5p/PIM3 axis represents a potential therapeutic target for ACS.