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Galectin-3-induced oxidized low-density lipoprotein promotes the phenotypic transformation of vascular smooth muscle cells.

Tian L, Chen K, Cao J, Han Z, Gao L, Wang Y, Fan Y, Wang C - Mol Med Rep (2015)

Bottom Line: The oxLDL‑induced cells exhibited increased expression levels of osteopontin, a smooth muscle synthetic protein, and calponin and α‑actin, smooth muscle contractile proteins.The oxLDL‑induced changes in cellular phenotype were associated with increased migration, proliferation, and phagocytosis.Concordant with these results, oxLDL‑treated smooth muscle cells exhibited activation of canonical Wnt signaling, as determined by an increase in the protein expression levels of β‑catenin.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200011, P.R. China.

ABSTRACT
Oxidized low-density lipoprotein (oxLDL) is involved in the pathological phenotypic transformation of vascular smooth muscle cells in atherosclerosis. Galectin‑3 also has an important role in atherosclerosis. However, little is currently known regarding the effects of galectin‑3 on the oxLDL‑induced phenotypic transformation of vascular smooth muscle cells. In the present study, primary culture human umbilical vascular smooth muscle cells were treated with various oxLDL concentrations (0‑50 µg/ml) for 72 h, and phenotypic changes were subsequently recorded. The results of the present study suggested that oxLDL increases the expression levels of galectin‑3, and induces the phenotypic transformation of vascular smooth muscle cells. The oxLDL‑induced cells exhibited increased expression levels of osteopontin, a smooth muscle synthetic protein, and calponin and α‑actin, smooth muscle contractile proteins. The oxLDL‑induced changes in cellular phenotype were associated with increased migration, proliferation, and phagocytosis. Concordant with these results, oxLDL‑treated smooth muscle cells exhibited activation of canonical Wnt signaling, as determined by an increase in the protein expression levels of β‑catenin. Silencing of galectin‑3 by small interfering RNA reversed the phenotypic transformation and functional changes observed in the oxLDL‑treated cells, suggesting these changes were dependent on the activation of galectin‑3. In addition, galectin‑3 knockdown decreased the protein expression levels of β‑catenin in both the cytoplasm and nucleus; however, the mRNA expression levels of β‑catenin remained unchanged. These results suggest that galectin‑3 is responsible for the phenotypic transformation of human umbilical vascular smooth muscle cells, and the canonical Wnt/β-catenin signaling pathway may be involved in this process.

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(A) Oxidized low-density lipoprotein (oxLDL) induces phenotypic changes in human umbilical smooth muscle cells (HUSMCs), and increases the expression levels of galectin-3 (gal-3). The cells were treated with various concentrations of oxLDL (0-50 μg/ml) for 48 h, and the expression levels of gal-3, calponin, smooth muscle α-actin (SMA), and osteopontin (OPN) were measured by western blotting. (B) The protein expression levels of GAPDH were used as a control. The respective densitometric measurement results are given, and the band intensities of the HUSMCs were defined by the control and set to 1. Data are presented as the mean ± standard deviation. *P<0.05, vs. the control.
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f1-mmr-12-04-4995: (A) Oxidized low-density lipoprotein (oxLDL) induces phenotypic changes in human umbilical smooth muscle cells (HUSMCs), and increases the expression levels of galectin-3 (gal-3). The cells were treated with various concentrations of oxLDL (0-50 μg/ml) for 48 h, and the expression levels of gal-3, calponin, smooth muscle α-actin (SMA), and osteopontin (OPN) were measured by western blotting. (B) The protein expression levels of GAPDH were used as a control. The respective densitometric measurement results are given, and the band intensities of the HUSMCs were defined by the control and set to 1. Data are presented as the mean ± standard deviation. *P<0.05, vs. the control.

Mentions: According to a previous study (17), minimally-oxidized LDL may induce phenotypic transformation of coronary artery smooth muscle cells. The present study demonstrated that oxLDL directly induced significant changes in smooth muscle cell phenotype, following cellular treatment with various oxLDL concentrations (0-50 μg/ml). Treatment with oxLDL induced a marked increase in the expression levels of smooth muscle synthetic related protein OPN, and contractile related proteins calponin and SMA. OxLDL also increased the protein expression levels of gal-3 (Fig. 1A and B).


Galectin-3-induced oxidized low-density lipoprotein promotes the phenotypic transformation of vascular smooth muscle cells.

Tian L, Chen K, Cao J, Han Z, Gao L, Wang Y, Fan Y, Wang C - Mol Med Rep (2015)

(A) Oxidized low-density lipoprotein (oxLDL) induces phenotypic changes in human umbilical smooth muscle cells (HUSMCs), and increases the expression levels of galectin-3 (gal-3). The cells were treated with various concentrations of oxLDL (0-50 μg/ml) for 48 h, and the expression levels of gal-3, calponin, smooth muscle α-actin (SMA), and osteopontin (OPN) were measured by western blotting. (B) The protein expression levels of GAPDH were used as a control. The respective densitometric measurement results are given, and the band intensities of the HUSMCs were defined by the control and set to 1. Data are presented as the mean ± standard deviation. *P<0.05, vs. the control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4581830&req=5

f1-mmr-12-04-4995: (A) Oxidized low-density lipoprotein (oxLDL) induces phenotypic changes in human umbilical smooth muscle cells (HUSMCs), and increases the expression levels of galectin-3 (gal-3). The cells were treated with various concentrations of oxLDL (0-50 μg/ml) for 48 h, and the expression levels of gal-3, calponin, smooth muscle α-actin (SMA), and osteopontin (OPN) were measured by western blotting. (B) The protein expression levels of GAPDH were used as a control. The respective densitometric measurement results are given, and the band intensities of the HUSMCs were defined by the control and set to 1. Data are presented as the mean ± standard deviation. *P<0.05, vs. the control.
Mentions: According to a previous study (17), minimally-oxidized LDL may induce phenotypic transformation of coronary artery smooth muscle cells. The present study demonstrated that oxLDL directly induced significant changes in smooth muscle cell phenotype, following cellular treatment with various oxLDL concentrations (0-50 μg/ml). Treatment with oxLDL induced a marked increase in the expression levels of smooth muscle synthetic related protein OPN, and contractile related proteins calponin and SMA. OxLDL also increased the protein expression levels of gal-3 (Fig. 1A and B).

Bottom Line: The oxLDL‑induced cells exhibited increased expression levels of osteopontin, a smooth muscle synthetic protein, and calponin and α‑actin, smooth muscle contractile proteins.The oxLDL‑induced changes in cellular phenotype were associated with increased migration, proliferation, and phagocytosis.Concordant with these results, oxLDL‑treated smooth muscle cells exhibited activation of canonical Wnt signaling, as determined by an increase in the protein expression levels of β‑catenin.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiology, Shanghai Ninth People's Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai 200011, P.R. China.

ABSTRACT
Oxidized low-density lipoprotein (oxLDL) is involved in the pathological phenotypic transformation of vascular smooth muscle cells in atherosclerosis. Galectin‑3 also has an important role in atherosclerosis. However, little is currently known regarding the effects of galectin‑3 on the oxLDL‑induced phenotypic transformation of vascular smooth muscle cells. In the present study, primary culture human umbilical vascular smooth muscle cells were treated with various oxLDL concentrations (0‑50 µg/ml) for 72 h, and phenotypic changes were subsequently recorded. The results of the present study suggested that oxLDL increases the expression levels of galectin‑3, and induces the phenotypic transformation of vascular smooth muscle cells. The oxLDL‑induced cells exhibited increased expression levels of osteopontin, a smooth muscle synthetic protein, and calponin and α‑actin, smooth muscle contractile proteins. The oxLDL‑induced changes in cellular phenotype were associated with increased migration, proliferation, and phagocytosis. Concordant with these results, oxLDL‑treated smooth muscle cells exhibited activation of canonical Wnt signaling, as determined by an increase in the protein expression levels of β‑catenin. Silencing of galectin‑3 by small interfering RNA reversed the phenotypic transformation and functional changes observed in the oxLDL‑treated cells, suggesting these changes were dependent on the activation of galectin‑3. In addition, galectin‑3 knockdown decreased the protein expression levels of β‑catenin in both the cytoplasm and nucleus; however, the mRNA expression levels of β‑catenin remained unchanged. These results suggest that galectin‑3 is responsible for the phenotypic transformation of human umbilical vascular smooth muscle cells, and the canonical Wnt/β-catenin signaling pathway may be involved in this process.

Show MeSH
Related in: MedlinePlus