title: Angiogenic signaling triggered by cariogenic bacteria in pulp cells.
abstract: The inflammation observed in the dental pulp of teeth with deep caries lesions is characterized by a significant increase in blood vessel density. It is known that lipoteichoic acid (LTA) from Gram-positive cariogenic bacteria induces expression of vascular endothelial growth factor (VEGF) in dental pulp cells. The hypothesis underlying this study was that LTA induces VEGF expression in dental pulp cells through TLR2 and PI3k/Akt signaling. Odontoblast-like cells (MDPC-23) and undifferentiated pulp cells (OD-21) were exposed to LTA from Streptococcus sanguis, and the role of TLR2, PI3K/Akt, and IKK signaling in LTA-induced VEGF expression was evaluated. These studies demonstrated that TLR2 signaling through the PI3K-Akt pathway is necessary for LTA-induced VEGF expression in pulp cells. In contrast, inhibition of IKK signaling did not prevent VEGF up-regulation in response to LTA. Understanding signaling pathways triggered by cariogenic bacteria may reveal novel therapeutic targets for the clinical management of pulpitis.
authors.affiliation: Department of Cariology, Restorative Sciences, and Endodontics, University of Michigan School of Dentistry, 1011 N. University, Rm. 2309, Ann Arbor, MI 48103-1078, USA.
authors.forename: R I
authors.initials: RI
authors.lastname: Soden
authors.forename: T M
authors.initials: TM
authors.lastname: Botero
authors.forename: C T
authors.initials: CT
authors.lastname: Hanks
authors.forename: J E
authors.initials: JE
authors.lastname: Nör
mesh_terms: D000818:Animals; D002460:Cell Line; D003731:Dental Caries / Q000382:microbiology*; D003782:Dental Pulp / Q000098:blood supply / Q000166:cytology / Q000382:microbiology*; D005347:Fibroblasts / Q000187:drug effects; D005881:Gingiva / Q000166:cytology / Q000187:drug effects; D051550:I-kappa B Kinase / Q000032:analysis / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects; D051379:Mice; D055806:Microvessels / Q000187:drug effects / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000502:physiology*; D009804:Odontoblasts / Q000187:drug effects; D019869:Phosphatidylinositol 3-Kinases / Q000032:analysis / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000032:analysis / Q000187:drug effects; D011671:Pulpitis / Q000382:microbiology / Q000473:pathology; D015398:Signal Transduction / Q000502:physiology*; D013298:Streptococcus sanguis / Q000502:physiology*; D013682:Teichoic Acids / Q000494:pharmacology; D051195:Toll-Like Receptor 2 / Q000032:analysis / Q000187:drug effects; D015854:Up-Regulation; D042461:Vascular Endothelial Growth Factor A / Q000032:analysis / Q000187:drug effects; D040301:Vascular Endothelial Growth Factor Receptor-2 / Q000032:analysis / Q000187:drug effects
chemical_list: D051550:I-kappa B Kinase; D008070:Lipopolysaccharides; D019869:Phosphatidylinositol 3-Kinases; D051057:Proto-Oncogene Proteins c-akt; D013682:Teichoic Acids; D051195:Toll-Like Receptor 2; D042461:Vascular Endothelial Growth Factor A; D040301:Vascular Endothelial Growth Factor Receptor-2; C493486:Tlr2 protein, mouse; C467480:vascular endothelial growth factor A, mouse; C009900:lipoteichoic acid; C496562:Ikbkb protein, mouse