Modulation of cell proliferation, survival and gene expression by RAGE and TLR signaling in cells of the innate and adaptive immune response: role of p38 MAPK and NF-KB

• Autor(a) principal: MEDEIROS,Marcell Costa de
• Data de Publicação: 2014
• Outros Autores: FRASNELLI,Sabrina Cruz Tfaile, BASTOS,Alliny de Souza, ORRICO,Silvana Regina Perez, ROSSA JUNIOR,Carlos
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Journal of applied oral science (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1678-77572014000300185
• topic: Periodontal diseases; Diabetes mellitus; Innate immunity; Acquired immunity; Advanced glycosylation end products

Objective: The aim of this study was to evaluate a possible synergism between AGE-RAGE and TLR4 signaling and the role of p38 MAPK and NF-kB signaling pathways on the modulation of the expression of inflammatory cytokines and proliferation of cells from the innate and adaptive immune response. Material and Methods: T lymphocyte (JM) and monocyte (U937) cell lines were stimulated with LPS and AGE-BSA independently and associated, both in the presence and absence of p38 MAPK and NF-kB inhibitors. Proliferation was assessed by direct counting and viability was assessed by a biochemical assay of mitochondrial function. Cytokine gene expression for RAGe, CCL3, CCR5, IL-6 and TNF-α was studied by RT-PCR and RT-qPCR. Results: RAGE mRNA expression was detected in both cell lines. LPS and AGE-BSA did not influence cell proliferation and viability of either cell line up to 72 hours. LPS and LPS associated with AGE induced expression of IL-6 and TNF-α in monocytes and T cells, respectively. Conclusions: There is no synergistic effect between RAGE and TLR signaling on the expression of IL-6, TNF-α , RAGE, CCR5 and CCL3 by monocytes and lymphocytes. Activation of RAGE associated or not with TLR signaling also had no effect on cell proliferation and survival of these cell types.