title: 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.
abstract: 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.
  
  
  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.
authors.forename: Marcell Costa de
authors.initials: MC
authors.lastname: Medeiros
authors.forename: Sabrina Cruz Tfaile
authors.initials: SC
authors.lastname: Frasnelli
authors.forename: Alliny de Souza
authors.initials: Ade S
authors.lastname: Bastos
authors.forename: Silvana Regina Perez
authors.initials: SR
authors.lastname: Orrico
authors.forename: Carlos
authors.initials: C
authors.lastname: Rossa
mesh_terms: D056704:Adaptive Immunity / Q000235:genetics / Q000276:immunology*; D017209:Apoptosis; D002460:Cell Line; D049109:Cell Proliferation; D002470:Cell Survival / Q000502:physiology; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D057075:Enzyme Assays; D015870:Gene Expression / Q000235:genetics*; D006801:Humans; D007113:Immunity, Innate / Q000235:genetics / Q000276:immunology*; D016328:NF-kappa B / Q000235:genetics* / Q000276:immunology; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction; D015398:Signal Transduction; D013997:Time Factors; D051197:Toll-Like Receptor 4 / Q000235:genetics* / Q000276:immunology; D048051:p38 Mitogen-Activated Protein Kinases / Q000502:physiology*
chemical_list: D016207:Cytokines; D016328:NF-kappa B; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic; D051197:Toll-Like Receptor 4; D048051:p38 Mitogen-Activated Protein Kinases