Porphyromonas gingivalis, periodontal pathogen, lipopolysaccharide induces angiogenesis via extracellular signal-regulated kinase 1/2 activation in human vascular endothelial cells.
Porphyromonas gingivalis is a major periodontal pathogen. The lipopolysaccharide (LPS) secreted from P. gingivalis is implicated in the initiation and progression of periodontitis. Aberrant angiogenesis is often associated with lesion formation in chronic periodontitis. In this study, we report that P. gingivalis LPS activates angiogenic cascade, migration, invasion and tube formation in human umbilical vein endothelial cells (HUVECs). Furthermore, P. gingivalis LPS potently stimulated in vivo neovascularization in chick chorioallantoic membrane (CAM) and the mouse Matrigel plug assay. P. gingivalis LPS had no effect on the expression of vascular endothelial growth factor (VEGF) or its receptor, Flk-1, implying that P. gingivalis LPS-induced angiogenesis may result from its direct action on endothelial cells. P. gingivalis LPS evoked activation of the mitogen-activated protein kinase ERK1/2 in HUVECs, which is closely linked to angiogenesis. Taken together, these results strongly suggest P. gingivalis LPS plays an important role in the pathological angiogenesis for periodontal diseases, such as periodontitis.
Koo
Tae Hyeon
TH
College of Dentistry and Research Institute for Oral Biotechnology, Pusan 602-739, Korea.
Jun
Hyung Oh
HO
Bae
Soo-Kyung
SK
Kim
Su-Ryun
SR
Moon
Chang-Pyo
CP
Jeong
Seong-Kyoon
SK
Kim
Woo-Sik
WS
Kim
Gyoo Cheon
GC
Jang
Hye-Ock
HO
Yun
Il
I
Kim
Kyu-Won
KW
Bae
Moon-Kyoung
MK
D000818:Animals; D002465:Cell Movement; D048430:Cell Shape; D002478:Cells, Cultured; D002642:Chick Embryo; D049033:Chorioallantoic Membrane / Q000098:blood supply / Q000378:metabolism; D003094:Collagen / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004338:Drug Combinations; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D004789:Enzyme Activation; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism*; D006801:Humans; D007797:Laminin / Q000378:metabolism; D008070:Lipopolysaccharides / Q000378:metabolism* / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000187:drug effects; D051379:Mice; D008810:Mice, Inbred C57BL; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009389:Neovascularization, Pathologic / Q000378:metabolism*; D010510:Periodontal Diseases / Q000378:metabolism / Q000382:microbiology; D010766:Phosphorylation; D016966:Porphyromonas gingivalis / Q000378:metabolism*; D011509:Proteoglycans / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000378:metabolism
D004338:Drug Combinations; D007797:Laminin; D008070:Lipopolysaccharides; D011509:Proteoglycans; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C059485:matrigel; D003094:Collagen; D040301:Vascular Endothelial Growth Factor Receptor-2; D048049:Extracellular Signal-Regulated MAP Kinases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3