title: Toll-like receptor 2 in promoting angiogenesis after acute ischemic             injury.
abstract: Angiogenesis is an important mechanism that protects tissue against necrosis             following acute ischemic injury. The aim of this study was to investigate whether             the Toll-like receptor 2 (TLR2) signaling pathway is involved in angiogenesis             following ischemic injury by cell migration and lymphocyte invasion assays in vitro,             and a mouse model of hindlimb ischemia by ligation in vivo, respectively. To assess             the potential role of TLR2 activation in endothelial cell permeability, HUVECs             were pretreated with Pam3CSK4 and analyzed using wound repair and transwell assays.             The results showed that the TLR2 agonist induced human umbilical vein endothelial             cell (HUVEC) migration and increased the permeability of HUVECs to lymphocyte.             The lymphocyte invasion of TLR2 knockout (TLR2-/-) mice was inhibited as compared             to that of wild-type (WT) mice. In the mouse model of hindlimb ischemia by ligation,             blood perfusion of operated limbs was significantly lower in TLR2-/- compared             to WT mice, 7 and 14 days after ligation. TLR2-/- mice showed a decreased CD31             expression in ischemic gastrocnemius at 7 and 14 days after ligation, reduced             interleukin-6 (IL-6) level and lowered tumor necrosis factor-α (TNF-α) levels.             These findings demonstrated that TLR2 activation promotes cell migration, cell             permeability and the lymphocyte invasion of endothelial cells. TLR2 activation             promotes angiogenesis in vivo, which may be associated with the serum of TNF-α             levels and IL-6 release.
authors: Department of Cardiology, The Second Affiliated Hospital, Zhejiang University College of Medicine, Hangzhou, Zhejiang 310009, PR China.
authors: Yifei
authors: Y
authors: Xu
authors: Ying
authors: Y
authors: Zhou
authors: Haiyan
authors: H
authors: Lin
authors: Haiyang
authors: H
authors: Hu
authors: Yuxing
authors: Y
authors: Wang
authors: Geng
authors: G
authors: Xu
mesh_terms: D000818:Animals; D017209:Apoptosis; D002465:Cell Movement; D002478:Cells, Cultured; D004789:Enzyme Activation; D006614:Hindlimb / Q000293:injuries / Q000601:surgery; D061307:Human Umbilical Vein Endothelial Cells / Q000378:metabolism*; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis; D007511:Ischemia; D055666:Lipopeptides; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D018482:Muscle, Skeletal / Q000293:injuries / Q000378:metabolism / Q000601:surgery*; D018919:Neovascularization, Physiologic / Q000235:genetics / Q000502:physiology*; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000096:biosynthesis; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
chemical_list: D015850:Interleukin-6; D055666:Lipopeptides; C508075:Pam(3)CSK(4) peptide; D019408:Platelet Endothelial Cell Adhesion Molecule-1; D051195:Toll-Like Receptor 2; D014409:Tumor Necrosis Factor-alpha