Galectin-3 Elicited By OxLDL Promotes The Phenotype Transformation Of Vascular Smooth Muscle Cells

Background Oxidized LDL(ox LDL) is involved in the phenotype transformation of vascular smooth muscle cells during the pathological process of atherosclerosis. Galectin-3 also plays an important role in atherosclerosis. However, notably little is known regarding the effect of galectin-3 in the ox LDL-induced phenotype transformation of vascular smooth muscle cells.Methods Primary VSMC was treated with ox LDL and galectin-3, and then cellular phenotype changes were investigated. The expression of galectin-3, OPN, SMA, calponin, ?-catenin and axin2 was tested by Realtime PCR and Western blot. Si RNA strategy was used to knockdown galectin-3 and ?-cateninResults ox LDL enhances the expression of galectin-3 and completely induces the phenotype transformation of vascular smooth muscle cells. The ox LDL-induced cells had increased expression of OPN, SMA and calponin and increased ability of migration and proliferation. Silencing of galectin-3 by small interfering RNA completely reversed the phenotype transformation observed in the ox LDL-treated cells, suggesting that these changes were dependent on the activation of galectin-3. The ox LDL-induced changes in cell phenotype were associated with the activation of canonical Wnt signalling, as measured by ?-catenin protein expression. We also observed that galectin-3 knockdown decreased the expression of ?-catenin protein in both the cytoplasm and the nucleus but not m RNA level. Exogenous galectin-3 promoted phenotype transformation of HUSMC. The galectin-3-induced changes in cell phenotype were associated with the activation of canonical Wnt signalling, as measured by ?-catenin and axin2 expression. ?-catenin inhibition by small interfering RNA reduced cell proliferation, decreased cell motility, and blocked galectin-3-induced phenotype transformation of HUSMC.Conclusion Our data suggest that ox LDL induces the phenotype transformation of human umbilical vascular smooth muscle cells via galectin-3. The canonical Wnt/?-catenin signalling pathway is believed to mediate this process.