Differential expression of mitogen activating protein kinases in periodontitis. (7th June 2013)

• Record Type: Journal Article
• Authors: Travan, Suncica; Li, Fei; D'Silva, Nisha J.; Slate, Elizabeth H.; Kirkwood, Keith L.
• Is Part Of: Journal of clinical periodontology. Volume 40:Number 8(2013:Aug.)
• Page Start: 757
• Page End: 764
• Publication Date: 2013-06-07
• Subjects: cell signalling -- inflammation -- mitogen activating protein kinases -- periodontitis; Periodontics -- Periodicals; 617.6
• DOI: 10.1111/jcpe.12123
• Languages: English
• ISSNs: 0303-6979

Abstract

Abstract: Aim: Following toll‐like receptor (TLR) engagement, lipopolysaccharide (LPS) can stimulate the expression of pro‐inflammatory cytokines thus activating the innate immune response. The production of inflammatory cytokines results, in part, from the activation of kinase‐induced signalling cascades and transcriptional factors. Of the four distinct classes of mitogen‐activated protein kinases (MAPK) described in mammals, p38, c‐Jun N‐terminal activated kinases (JNK1‐3) and extracellular activated kinases (ERK1, 2) are the best studied. Previous data have established that p38 MAPK signalling is required for inflammation and bone loss in periodontal disease pre‐clinical animal models. Materials & Methods: In this study, we obtained healthy and diseased periodontal tissues along with clinical parameters and microbiological parameters. Excised fixed tissues were immunostained with total and phospho‐specific antibodies against p38, JNK and ERK kinases. Results: Intensity scoring from immunostained tissues was correlated with clinical periodontal parameters. Rank correlations with clinical indices were statistically significantly positive ( p ‐value < 0.05) for total p38 (correlations ranging 0.49–0.68), phospho‐p38 (range 0.44–0.56), and total ERK (range 0.52–0.59) levels, and correlations with JNK levels also supported association (range 0.42–0.59). Phospho‐JNK and phospho‐ERK showed no significant positive correlation with clinical parameters of disease. Conclusion: These data strongly implicate p38 MAPK as a major MAPK involved in human periodontal inflammation and severity.