Higher Adiponectin Expression Suppresses Neointimal Hyperplasia by Attenuating the Inflammatory Response Following Acceleration of Endothelialization in Damaged Areas in Adiponectin Transgenic Mice

Abstract

Adiponectin prevents inflammation and atherosclerosis, but it is unclear whether overexpression of adiponectin protects the vasculature. The aim of the present study was to determine whether adiponectin overexpression promotes vascular repair after mechanical injury using adiponectin transgenic (Tg) mice. Studies were performed in 7–8-week-old C57/BL6 (wild-type; WT; n=50) and adiponectin Tg (n=46) mice. A damaged endothelium model was created by inserting a large wire into the femoral artery. Von Willebrand factor-positive cells were observed on the surface of the damaged area from 1 week after wire injury in Tg mice, and from 2 weeks in WT mice. At 1 week, both α-smooth muscle embryonic myosin heavy chain-positive cells and intercellular adhesion molecule-positive cells were observed in the neointima in WT but not Tg mice. The intima/media ratio was significantly smaller in Tg than WT mice. Adiponectin and tumor necrosis factor (TNF)-α mRNA expression was observed in non-injured Tg and WT mice, but serum and mesenteric adipose tissue adiponectin concentrations were significantly higher in Tg than WT mice. Higher adiponectin and lower TNF-α levels, brought about by adiponectin transgene expression, suppressed neointimal hyperplasia by attenuating the inflammatory response following the acceleration of endothelialization in damaged areas in adiponectin Tg mice.