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. Author manuscript; available in PMC: 2011 Jun 1.
Published in final edited form as: Int J Biochem Cell Biol. 2010 Feb 23;42(6):965–974. doi: 10.1016/j.biocel.2010.02.009

Figure 1. Hyperglycemia promotes SMC growth, proliferation, and the development of intimal hyperplasia in an integrin β3-dependent manner.

Figure 1

Representative combined Masson elastic stained sections of femoral arteries of diabetic wild-type (WT) or Itgβ3−/− four weeks after wire-induced endothelial denuduation (A; 20x). Isolated murine SMCs (20 000 cells) were cultured in euglycemic (5 mM; open bars) or hyperglycemic (25 mM; dark bars) conditions with the indicated inhibitors for 48 hours. Cell proliferation was measured by WST-1 assay kit, and the results are presented as mean ± SE from three independent experiments (B). Migration of SMCs was performed in euglycemic (5 mM; open bar) or hyperglycemic (25 mM; dark bars) conditions with the indicated inhibitors. Inhibitors used were as follows: PKCβ (3-(1-(3-Imidazol-1-ylpropyl)-1H-indol-3-yl)-4-anilino-1H-pyrrole-2,5-dione, 5nM), anti-β3 antibody (10 µg/ml), control antibody (10 µg/ml). Cell migration was measured as described in Methods, and the results are presented as mean ± SE from three independent experiments (C). *P < 0.001 as compared to corresponding control.