Abstract
Abdominal aortic aneurysm (AAA) is a chronic vascular inflammatory disease. The regulatory mechanisms during AAA formation remain unclear. Bone marrow stem cells (BMSCs) are pluripotent cells capable of regulating the progression of various diseases by delivering exosomes and exosomal lncRNAs. In this study, we investigated its function in AAA by isolating BMSC exosome-derived lncRNA SBF2-AS1. The results showed that BF2-AS1 could be transferred to vascular smooth muscle cells (VSMCs) and human aortic VSMCs (HASMCs) via BMSC-derived exosomes. Depletion of SBF2-AS1 enhanced the cell viability and proliferation of VSMCs. Conversely, SBF2-AS1 knockdown inhibited VSMC apoptosis. Caspase-3 activity was inhibited by depletion of SBF2-AS1, whereas overexpression of SBF2-AS1 in VSMC promoted Caspase-3 activity. SBF2-AS1 enhances SMARCD1 expression by forming miR-520f-3p in VSMC and HASMC. Overexpression of SMARCD1 or miR-520f-3p inhibitor reversed cell viability and caspase-3 activity mediated by SBF2-AS1 depletion in VSMC and HASMC. Therefore, BMSC exosome-derived SBF2-AS1 promotes AAA formation through the miRNA-520f-3p/SMARCD1 axis. Targeting SBF2-AS1 could serve as a promising therapeutic strategy for AAA.