SNHG16 suppression enhances M2 macrophage polarization and inhibits VSMC migration in atherosclerosis.

Atherosclerosis (AS) significantly impacts both cardiovascular and cerebrovascular health, making it an important area of research for potential therapeutic interventions. This study investigates the role of lncRNA SNHG16 in macrophage polarization and its effects on the progression of AS. We assessed the expression of SNHG16 in macrophages and vascular smooth muscle cells (VSMCs) treated with oxidized low-density lipoprotein (ox-LDL) using qPCR. Cell proliferation was evaluated via EdU assay and western blotting, while flow cytometry and immunofluorescence were employed to analyze the polarization of macrophages. Foam cell formation was examined using Oil Red O staining. In a co-culture system, VSMCs treated with ox-LDL were cultured alongside macrophages pretreated with sh-SNHG16, and VSMC viability, migration, and motility were assessed using CCK-8, migration, and scratch assays. The levels of inflammatory cytokines, including IL-6, IL-10, TGFβ, and TNFα, were quantified by ELISA. Our results show that SNHG16 expression is upregulated in ox-LDL-treated cells, which correlates with enhanced macrophage proliferation. Inhibition of SNHG16 promoted M1-to-M2 macrophage polarization, reducing foam cell formation and inflammation. Furthermore, SNHG16 knockdown limited VSMC viability and motility, while attenuating ox-LDL-induced inflammatory responses. In conclusion, suppression of SNHG16 favors M2 macrophage polarization and presents a potential therapeutic target for AS management.