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Role of Protease-Activated receptor 2 (PAR2) during Porphyromonas gingivalis infection on the regulation of p38-MAPK signaling in periodontal cells

Grant number: 12/22439-1
Support Opportunities:Scholarships abroad - Research Internship - Doctorate
Effective date (Start): February 20, 2013
Effective date (End): February 19, 2014
Field of knowledge:Health Sciences - Dentistry - Periodontology
Principal Investigator:Marinella Holzhausen Caldeira
Grantee:Vanessa Tubero Euzebio Alves
Supervisor: Ibrahim Alpdogan Kantarci
Host Institution: Faculdade de Odontologia (FO). Universidade de São Paulo (USP). São Paulo , SP, Brazil
Research place: Forsyth Institute, United States  
Associated to the scholarship:10/20477-8 - Evaluation of the protease activated receptor 2(PAR-2) expression in chronic periodontitis patients, before and after non-surgical periodontal treatment, BP.DR


The association of Protease-activated receptor 2 (PAR2) and periodontitis was first suggested by in vitro studies which demonstrated that osteoblasts, oral epithelial cells and human gingival fibroblasts can express PAR2. Furthermore, it was observed that a selective agonist of PAR2 causes gingival granulocyte infiltration in rats and PAR2-deficient (PAR2-/-) mice show less inflammation resulting from infection by Porphyromonas gingivalis (P. gingivalis). In addition, in a recent study (Holzhausen et al., 2010) it was observed that patients with chronic periodontitis present an increase in PAR2 expression in the oral crevicular fluid compared to periodontally healthy patients. However, the immunoinflammatory mechanisms by which PAR2 activation can lead to greater periodontal destruction still deserve to be elucidated. Thereby this study aims to investigate the role of PAR2 and the mitogen activated protein kinase (MAPK) signaling pathway in the production of pro-inflammatory cytokines by human periodontal cells during Porphyromonas gingivalis infection. It will be performed an in vitro study and p38-MAPK signaling pathway via PAR2 will be evaluate in oral epithelial cells and neutrophils during P. gingivalis infection. PAR2 mRNA will be evaluated in neutrophils and epithelial cells by Real-Time PCR and a possible involvement of the p-38 MAPK signaling pathway will be assessed by Western Blot. Thus it will be evaluated the correlation between p-38 MAPK expression and the release of pro-inflammatory mediators after PAR2 activation, in periodontal human cells infected by P. gingivalis. We expected that, during infection by Porphyromonas gingivalis, it will be observed a positive correlation between the activation of PAR2 expression and MAPK signaling pathway. (AU)

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