Galectin-3 induces the phenotype transformation of human vascular smooth muscle cells via the canonical Wnt signaling

Abstract

Galectin‑3, a galactoside‑binding protein, is highly expressed in carotid plaques and plays an important role in the atherosclerotic lesions. The phenotype transformation of vascular smooth muscle cells is the basic pathological change of atherosclerosis. This study investigated the effects of exogenous galectin‑3 on the function and phenotype transformation of human umbilical vascular smooth muscle cells (HUSMC). In this study, we treated vascular smooth muscle cells with recombinant galectin‑3 and tested its effect on cell proliferation, migration, and phenotype transformation. Our results showed that exogenous galectin‑3 promoted human umbilical vascular smooth muscle cells (HUSMC) proliferation and migration. Exogenous galectin‑3 enhanced the expression of the smooth muscle synthetic protein osteopontin, smooth muscle contractile proteins calponin and smooth muscle α‑actin. The galectin‑3‑induced change in cell phenotype was associated with the activation of canonical Wnt signaling, as measured by β‑catenin axin2 and cyclin D1 expression. β‑catenin inhibition by small interfering RNA reduced cell proliferation, decreased cell motility, and blocked galectin‑3‑induced phenotype transformation of human umbilical vascular smooth muscle cells (HUSMC). Our data suggest galectin‑3 promotes the phenotype transformation of human umbilical vascular smooth muscle cells (HUSMC) by activating Wnt/β‑catenin signaling pathway.

Galectin-3 Mediates Thrombin-Induced Vascular Smooth Muscle Cell Migration

“…Numerous studies have demonstrated that thrombin promotes cellular migration (25,26). Gal-3 is an anti-adhesive factor that promotes SMC migration and may accelerate atherogenesis (16,27). In our research, we found that thrombin increased gal-3 expression.…”

“…Acute MI increases gal-3 level, which is positively correlated with left ventricular ejection fraction (LVEF) (14,15). Besides, in our previous research, gal-3 was found to promote VSMC migration via the Wnt/β-catenin signaling pathway (16).…”

Galectin-3 Is a Potential Mediator for Atherosclerosis

“…Tian et al reported that Gal-3 expression increased in the phenotypic transformed VSMC treated with ox-LDL. Small interfering RNA silencing or knockdown of Gal-3 inhibited the phenotypic transformation and migration of VSMC[48], and another study of Tian et al particularly indicated that exogenous Gal-3 promoted human VSMC proliferation and migration through the activation of canonical Wnt/β-catenin signaling pathway[49].…”

Correlation between Galectin-3 and Adverse Outcomes in Myocardial Infarction Patients: A Meta-Analysis

“…Oxidized low-density lipoprotein (oxLDL) increases the expression of gal3 in VSMCs [4]. Gal3 also induces fibroblast and VSMCs to proliferate and produce fibrosis-related proteins in the extracellular matrix [8,9]. Strategies to inhibit gal3 induce decreased atherosclerosis and may reduce plaque progression [7,10].…”