LncRNA BANCR/miR-15a/MAPK1 Induces Apoptosis and Increases Proliferation of Vascular Smooth Muscle Cells in Aortic Dissection by Enhancing MMP2 Expression.

Aortic dissection is associated with a high mortality rate, contributing to an unfavorable prognosis. Preventive measures are more effective than therapeutic interventions for aortic dissection. While LncRNA BANCR is recognized as a functional translational regulator in various diseases, its role in aortic dissection remains unexplored. This study aims to elucidate the functions and molecular mechanisms of BANCR in aortic dissection. Vascular smooth muscle cells were isolated from dissected aortic tunica media samples and their phenotypes were compared with those of commercial vascular smooth muscle cells. BANCR expression was modulated via transient transfection (overexpression) and small interfering RNA (knockdown). The involvement of the p38 MAPK pathway was examined using the inhibitor SB202190. The competing endogenous RNA network was validated through a dual luciferase assay. Cellular phenotypes were assessed using the CCK-8 assay, scratch assay, and flow cytometry. BANCR was overexpressed in dissected aortic tissues and isolated vascular smooth muscle cells. MiR-15a-5p exhibited binding affinity to both BANCR and MAPK1. Overexpression of BANCR activated p38 phosphorylation, enhanced cell proliferation and migration, and increased apoptosis. SB202190 mitigated these BANCR-induced phenotypes by inhibiting p38 phosphorylation. Additionally, MMP2 upregulation was linked to BANCR overexpression via the p38 MAPK pathway. Suppression of BANCR expression or inhibition of p38 phosphorylation reduced MMP2 levels, thereby reversing BANCR-induced phenotypes. The LncRNA BANCR/miR-15a-5p/MAPK1 axis forms a ceRNA network that modulates MMP2 expression through the p38 MAPK signaling pathway in vascular smooth muscle cells. BANCR overexpression activates p38 MAPK phosphorylation, leading to enhanced MMP2 expression and subsequent increases in cell proliferation, migration, and apoptosis.