By modulating miR-525-5p/Bax axis, LINC00659 promotes vascular endothelial cell apoptosis

Area of Science:

• Molecular Biology
• Vascular Biology
• Genetics

Background:

• Deep vein thrombosis (DVT) is a significant vascular disease lacking effective treatments.
• Endothelial cells are critical in vascular injury response, thrombus formation, and hemostasis.
• Understanding molecular mechanisms in endothelial cells is key to developing DVT therapies.

Purpose of the Study:

• To investigate the role and mechanism of long noncoding RNA LINC00659 in endothelial cells.
• To elucidate the regulatory pathway involving LINC00659, miR-525-5p, and apoptosis markers in human umbilical vein endothelial cells (HUVECs).

Main Methods:

• Cell transfection assays were used to study LINC00659 and miR-525-5p functions in HUVECs.
• RT-qPCR and Western blot assessed expression levels of LINC00659, miR-525-5p, and apoptosis markers (Bcl-2, Bax).
• Bioinformatics, dual-luciferase reporter assays, MTT assays, and flow cytometry were employed to validate interactions and assess cellular effects.

Main Results:

• LINC00659 directly targets and downregulates miR-525-5p; miR-525-5p targets and downregulates Bax.
• Upregulation of LINC00659 inhibited HUVEC proliferation and promoted apoptosis.
• Silencing LINC00659 increased HUVEC viability and inhibited apoptosis by upregulating miR-525-5p and downregulating Bax.

Conclusions:

• LINC00659 plays a crucial role in regulating vascular endothelial cell apoptosis.
• The LINC00659/miR-525-5p/Bax axis is a key regulatory pathway in endothelial cells.
• Targeting this axis may offer a novel therapeutic strategy for deep vein thrombosis.