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Effect of PGC-1α on proliferation, migration, and transdifferentiation of rat vascular smooth muscle cells induced by high glucose.

Qi X, Zhang Y, Li J, Hou D, Xiang Y - J. Biomed. Biotechnol. (2012)

Bottom Line: We found that high glucose stimulated proliferation, migration and inflammatory gene expression of VSMCs, but overexpression of PGC-1α attenuated the effects of glucose.In addition, overexpression of PGC-1α decreased mRNA and protein level of VSMCs-related genes, and induced macrophage-related gene expression, as well as phagocytosis of VSMCs.Such transdifferentiation possibly increased the portion of VSMCs-derived foam cells in the plaque and favored plaque stability.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Diabetes Center, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.

ABSTRACT
We assessed the role of PGC-1α (PPARγ coactivator-1 alpha) in glucose-induced proliferation, migration, and inflammatory gene expression of vascular smooth muscle cells (VSMCs). We carried out phagocytosis studies to assess the role of PGC-1α in transdifferentiation of VSMCs by flow cytometry. We found that high glucose stimulated proliferation, migration and inflammatory gene expression of VSMCs, but overexpression of PGC-1α attenuated the effects of glucose. In addition, overexpression of PGC-1α decreased mRNA and protein level of VSMCs-related genes, and induced macrophage-related gene expression, as well as phagocytosis of VSMCs. Therefore, PGC-1α inhibited glucose-induced proliferation, migration and inflammatory gene expression of VSMCs, which are key features in the pathology of atherosclerosis. More importantly, PGC-1α transdifferentiated VSMCs to a macrophage-like state. Such transdifferentiation possibly increased the portion of VSMCs-derived foam cells in the plaque and favored plaque stability.

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Overexpression of PGC-1α inhibited proliferation, migration, and inflammatory gene expression of VSMCs in high glucose. VSMCs cultured in high-glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. (a) Proliferation of VSMCs, (b) migration of VSMCs, (c) inflammatory gene expression of VSMCs (*P < 0.05), and (d) Western blotting analysis for PGC-1α in VSMCs.
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fig2: Overexpression of PGC-1α inhibited proliferation, migration, and inflammatory gene expression of VSMCs in high glucose. VSMCs cultured in high-glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. (a) Proliferation of VSMCs, (b) migration of VSMCs, (c) inflammatory gene expression of VSMCs (*P < 0.05), and (d) Western blotting analysis for PGC-1α in VSMCs.

Mentions: VSMCs cultured in high glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. In proliferation and inflammatory gene expression assays, VSMCs were incubated by complete media for 6 h (Figures 2(a) and 2(c)). In migration assays, VSMCs were suspended and then high-glucose complete media was added to the lower compartment (Figure 2(b)). Results showed that proliferation, migration, and inflammatory gene expression of VSMCs were inhibited. Expression of PGC-1α in VSMCs treated with adenovirus infection was showed in Figure 2(d).


Effect of PGC-1α on proliferation, migration, and transdifferentiation of rat vascular smooth muscle cells induced by high glucose.

Qi X, Zhang Y, Li J, Hou D, Xiang Y - J. Biomed. Biotechnol. (2012)

Overexpression of PGC-1α inhibited proliferation, migration, and inflammatory gene expression of VSMCs in high glucose. VSMCs cultured in high-glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. (a) Proliferation of VSMCs, (b) migration of VSMCs, (c) inflammatory gene expression of VSMCs (*P < 0.05), and (d) Western blotting analysis for PGC-1α in VSMCs.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3303719&req=5

fig2: Overexpression of PGC-1α inhibited proliferation, migration, and inflammatory gene expression of VSMCs in high glucose. VSMCs cultured in high-glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. (a) Proliferation of VSMCs, (b) migration of VSMCs, (c) inflammatory gene expression of VSMCs (*P < 0.05), and (d) Western blotting analysis for PGC-1α in VSMCs.
Mentions: VSMCs cultured in high glucose (25 mmol/L) complete media were deprived of serum for 24 h. The cells were then treated with adenovirus infection for 48 h. In proliferation and inflammatory gene expression assays, VSMCs were incubated by complete media for 6 h (Figures 2(a) and 2(c)). In migration assays, VSMCs were suspended and then high-glucose complete media was added to the lower compartment (Figure 2(b)). Results showed that proliferation, migration, and inflammatory gene expression of VSMCs were inhibited. Expression of PGC-1α in VSMCs treated with adenovirus infection was showed in Figure 2(d).

Bottom Line: We found that high glucose stimulated proliferation, migration and inflammatory gene expression of VSMCs, but overexpression of PGC-1α attenuated the effects of glucose.In addition, overexpression of PGC-1α decreased mRNA and protein level of VSMCs-related genes, and induced macrophage-related gene expression, as well as phagocytosis of VSMCs.Such transdifferentiation possibly increased the portion of VSMCs-derived foam cells in the plaque and favored plaque stability.

View Article: PubMed Central - PubMed

Affiliation: Jiangsu Diabetes Center, State Key Laboratory of Pharmaceutical Biotechnology, School of Life Sciences, Nanjing University, Nanjing, China.

ABSTRACT
We assessed the role of PGC-1α (PPARγ coactivator-1 alpha) in glucose-induced proliferation, migration, and inflammatory gene expression of vascular smooth muscle cells (VSMCs). We carried out phagocytosis studies to assess the role of PGC-1α in transdifferentiation of VSMCs by flow cytometry. We found that high glucose stimulated proliferation, migration and inflammatory gene expression of VSMCs, but overexpression of PGC-1α attenuated the effects of glucose. In addition, overexpression of PGC-1α decreased mRNA and protein level of VSMCs-related genes, and induced macrophage-related gene expression, as well as phagocytosis of VSMCs. Therefore, PGC-1α inhibited glucose-induced proliferation, migration and inflammatory gene expression of VSMCs, which are key features in the pathology of atherosclerosis. More importantly, PGC-1α transdifferentiated VSMCs to a macrophage-like state. Such transdifferentiation possibly increased the portion of VSMCs-derived foam cells in the plaque and favored plaque stability.

Show MeSH
Related in: MedlinePlus