dc.contributorUniversidade Estadual Paulista (Unesp)
dc.creatorMedeiros, Marcell Costa de [UNESP]
dc.creatorTfaile Frasnelli, Sabrina Cruz [UNESP]
dc.creatorBastos, Alliny de Souza [UNESP]
dc.creatorOrrico, Silvana Regina Perez [UNESP]
dc.creatorRossa Júnior, Carlos [UNESP]
dc.date2014-12-03T13:10:46Z
dc.date2014-12-03T13:10:46Z
dc.date2014-05-01
dc.date.accessioned2023-09-09T10:00:15Z
dc.date.available2023-09-09T10:00:15Z
dc.identifierhttp://dx.doi.org/10.1590/1678-775720130593
dc.identifierJournal Of Applied Oral Science. Bauru-sp: Univ Sao Paulo Fac Odontologia Bauru, v. 22, n. 3, p. 185-193, 2014.
dc.identifier1678-7757
dc.identifierhttp://hdl.handle.net/11449/112501
dc.identifier10.1590/1678-775720130593
dc.identifierS1678-77572014000300185
dc.identifierWOS:000337907600008
dc.identifierS1678-77572014000300185.pdf
dc.identifier7383391319292040
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8762127
dc.descriptionObjective: 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-alpha 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-alpha in monocytes and T cells, respectively. Conclusions: There is no synergistic effect between RAGE and TLR signaling on the expression of IL-6, TNF-alpha, 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.
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionUniv Estadual Paulista, UNESP, Sch Dent, Dept Diag & Surg, Araraquara, SP, Brazil
dc.descriptionUniv Estadual Paulista, UNESP, Sch Dent, Dept Diag & Surg, Araraquara, SP, Brazil
dc.descriptionCAPES: 4638-05
dc.descriptionFAPESP: 10/06589-8
dc.format185-193
dc.languageeng
dc.publisherUniversidade de São Paulo (USP), Faculdade de Odontologia de Bauru
dc.relationJournal of Applied Oral Science
dc.relation1.709
dc.relation0,645
dc.rightsAcesso aberto
dc.sourceWeb of Science
dc.subjectPeriodontal diseases
dc.subjectDiabetes mellitus
dc.subjectInnate immunity
dc.subjectAcquired immunity
dc.subjectAdvanced glycosylation end products
dc.titleModulation 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
dc.typeArtigo


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