Background: Adiponectin has been reported to accumulate in the human injured artery and regulate the development of atherosclerosis, decreasing the expression of adhesion molecules in vascular endothelial cells, and inhibiting the proliferation of vascular smooth muscle cells. However, the role of adiponection after vascular injury is not fully elucidated. Therefore, we investigate whether adiponectin prevents neointimal hyperplasia after vascular injury in adiponectin transgenic mice (TG).
Methods: C57/BL6 mice (WT) and TG of 6 –7 week age were used. We inserted a large wire (0.38 mm in diameter) into femoral artery from distal side to proximal side to make the vascular endothelium damaged model. Mice were sacrificed at 1, 2 and 4 weeks, and non injured mice were used as control. Tissue concentration of fat and liver and serum concentration of adiponectin was measured using ELISA. Intima/ media ratio was measured in morphometrical analysis. Immunohistochemical staining of anti-adiponectin, anti-α-smooth muscle embryo (α-SMemb), anti-α-smooth muscle cell actin, von Willebrand Factor (vWF) and intercellular adhesion molecule-1 (ICAM-1) was performed using paraffin embedded sections.
Result: In immunohistochemical analysis at 1 week, α-SMemb positive cells, which were also positive for ICAM-1 were observed in WT, but were not seen in TG. Adiponectin positive cells, which were also positive for vWF were observed in the endothelial cells in TG, but were not detected in WT at 1 week, but those cells were observed in th endothelial cells in TG and WT at 2 and 4 weeks. In α-SMA staining at 4 weeks most neointimal area was stained with this anti-body in TG. On the other hand, in neointima of WT, only some area was stained with this anti-body. In morphometrical analysis, intima/media ratio was significantly smaller in TG than in WT at 1, 2 and 4 weeks. Adiponectin concentration of fat, liver and serum was significantly higher in TG than in WT in non-injured model and at 4 weeks. At 1 week liver and fat adiponectin level is significantly higher in TG than in WT, and serum adiponectin level in TG tended to be high as compared to that of WT.
Conclusions: Adiponectin prevents neointimal hyperplasia after vascular injury, probably through the inhibition of inflammatory reaction.
Altered Sca-1+ Progenitor Cell Populations in Diabetic Mice Are Associated with Increased Neointimal Hyperplasia After Vascular Injury
