BASP1, targeted by miR-185-5p, promotes atherosclerosis via VSMC proliferation and inflammation

To investigate the functional role and regulatory mechanisms of brain acid-soluble protein 1 (BASP1) in atherosclerosis (AS).

qRT-PCR was performed to detect BASP1 and miR-185-5p expression in the serum of healthy subjects and AS patients. Human umbilical artery smooth muscle cells (HUASMCs) were exposed to oxidized low-density lipoprotein (ox-LDL) to induce an AS cell model. The target binding relationship between BASP1 and miR-185-5p was verified by luciferase reporter gene assay and qRT-PCR. The effects of BASP1 on ox-LDL-induced proliferation, apoptosis and inflammation were evaluated through a series of in vitro assays. Rescue experiments were conducted to analyze the functional regulation of miR-185-5p by BASP1.

BASP1 expression was significantly elevated in the serum of AS patient and in ox-LDL-treated HUASMCs. Silencing BASP1 or overexpressing miR-185-5p reduced cell proliferation, apoptosis, inflammation, and adhesion molecule expression (vascular cellular adhesion molecule-1 (VCAM-1) and Intercellular adhesion molecule 1 (ICAM-1)). miR-185-5p directly targeted and negatively regulated BASP1. BASP1 overexpression partially reversed the effects of miR-185-5p mimics on ox-LDL-induced proliferation, apoptosis, inflammation, and adhesion molecule expression.

BASP1 may promote ox-LDL-induced proliferation and apoptosis in HUASMCs. The miR-185-5p/BASP1 molecular axis represents a promising target for the prevention and treatment of AS.