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(es)

de Medeiros, Marcell Costa ^[1] ; Tfaile Frasnelli, Sabrina Cruz ^[1] ; Bastos, Alliny de Souza ^[1] ; Perez Orrico, Silvana Regina ^[1] ; Rossa Junior, Carlos ^[1]

Afiliação do(s) autor(es)

^[1] Univ Estadual Paulista, UNESP, Sch Dent, Dept Diag & Surg, Araraquara, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Applied Oral Science; v. 22, n. 3, p. 185-193, MAY-JUN 2014.
• Citações Web of Science: 31

Resumo

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. (AU)

• Processo FAPESP: 10/06589-8 - Efeito da peroxidação de lípides, associado ou não à glicação de proteína, sobre a sinalização e expressão de marcadores inflamatórios
• Beneficiário: Carlos Rossa Junior
• Modalidade de apoio: Auxílio à Pesquisa - Regular