Angiogenesis is of great importance to a variety of normal physiological processes and pathological disorders.It is tightly regulated by many mechanisms, among which vascular endothelial growth factor(VEGF) is one of the most potent promoters.VEGF binds and activates its specific receptor tyrosine kinases, especially vascular endothelial growth factor receptor-2(VEGFR-2).VEGFR-2 mediates the key functional and biochemical effects of VEGF in endothelial cells including proliferation, migration, survival, and permeability.Following its binding to VEGF, VEGFR-2 dimerizes and undergoes autophosphorylation on tyrosine residues within its cytoplasmic portion.This creates docking sites for adapter molecules to be recruited through their Src homology domain-2(SH2).These adapter molecules can then initiate the activation of downstream signaling cascades.Further down-stream effector molecules are activated, and regulate the biological effects of endothelial cells.It is also foound that VEGF/VEGFR-2 signaling pathway may negatively regulate the function of human monocyte-derived mature dendritic cells(DCs) as well as the maturation of immature-DCs.Advances in the understanding of the VEGF/VEGFR-2 signaling pathway may contribute to the discovery of kinds of pharmaceutical agents.

Objective: To invesitgate the protein expression for leptin receptor in skeletal muscle in periodontitis and obese rat models, with the aim of exploring the effect of experimental periodontitis on adipokines receptors in insulin-targeting tissues and underlying mechanisms of skeletal muscle insulin resistance. Methods : Forty natal SD male rats were randomly divided into four groups, respectively: obese rats with periodontitis (OB+ CP group), obese rats without periodontitis (OB group), normal rats with periodontitis (CP group) and normal rats without periodontitis (C group). Obese rat model was established by subcutaneous injection of sodium glutamate. Experimental periodontitis was induced by ligation and inoculation of periodontal pathogens. Immunohistochemical analysis of leptin receptor expression in skeletal muscle of four groups was employed. Results: In the skeletal muscle, the protein for leptin receptor in the C group and CP group were popular and strong positive, and there was no statistically significant difference between the groups (P > 0.05). The protein expressions in the OB + CP group and OB group were decreased. Fewer protein expres⁃ sion was detected in the OB + CP group when compared with OB group (P < 0.05). A synergistic interaction between obesity and periodontitis was evident to the expression for the leptin receptor (P < 0.05). Conclusion Local infection induced by experimental periodontitis can barely down⁃regulate the protein expression for leptin receptor in the skeletal muscle. However, periodontitis can significantly down⁃regulate the protein expressions with the presence of obesity.