Relevance of the Myeloid Differentiation Factor 88 (MyD88) on RANKL, OPG, and Nod Expressions Induced by TLR and IL-1R Signaling in Bone Marrow Stromal Cells

dc.contributorUniversidade Federal de Pernambuco (UFPE)
dc.contributorUniversidade Estadual Paulista (Unesp)
dc.contributorUniversidade de São Paulo (USP)
dc.creatorManzolli Leite, Fabio Renato [UNESP]
dc.creatorAquino, Sabrina Garcia de [UNESP]
dc.creatorGuimaraes, Morgana Rodrigues [UNESP]
dc.creatorCirelli, Joni Augusto [UNESP]
dc.creatorZamboni, Dario S.
dc.creatorSilva, Joao S.
dc.creatorRossa Junior, Carlos [UNESP]
dc.date2015-10-21T13:10:39Z
dc.date2015-10-21T13:10:39Z
dc.date2015-02-01
dc.date.accessioned2023-09-12T06:36:05Z
dc.date.available2023-09-12T06:36:05Z
dc.identifierInflammation, v. 38, n. 1, p. 1-8, 2015.
dc.identifier0360-3997
dc.identifierhttp://hdl.handle.net/11449/128525
dc.identifier10.1007/s10753-014-0001-4
dc.identifierWOS:000349015900001
dc.identifier2628593693450121
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8777876
dc.descriptionThe myeloid differentiation factor 88 (MyD88) plays a pivotal role in Toll-like receptor (TLR)- and interleukin-1 receptor (IL-1R)-induced osteoclastogenesis. We examined the role of MyD88 on p38 mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kappa B) activation and nucleotide-binding oligomerization domain (Nod) induction by lipopolysaccharide (LPS) and IL-1 beta, and their effect on receptor activator of NF-kappa B ligand (RANKL) and osteoprotegerin (OPG) production in bone marrow stromal cell (BMSC). RANKL, Nod1, Nod2, NF-kappa B, and p38 protein levels were determined by Western blot. Nod2 was stimulated with muramyl dipeptide (MDP) prior to TLR4 stimulation with LPS. MyD88 deficiency markedly inhibited RANKL expression after LPS stimulation and increased OPG messenger RNA (mRNA) production. Also, MyD88 was necessary for NF-kappa B and p38 MAPK activation. MDP alone did not induce RANKL and OPG expressions; however, when combined with LPS, their expressions were significantly increased (p < 0.05). Our results support that MyD88 signaling has a pivotal role in osteoclastogenesis thought NF-kappa B and p38 activation. Nod2 and especially Nod1 levels were influenced by MyD88.
dc.descriptionCoordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.descriptionFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.descriptionFed Univ Pelotas UFPel, Sch Dent, Pelotas, RS, Brazil
dc.descriptionState Univ Sao Paulo UNESP, Dept Diag &Surg, Sch Dent Araraquara, BR-14801903 Sao Paulo, Brazil
dc.descriptionUniv Sao Paulo, Dept Cell Biol &Microbial Pathogenesis, Sch Med, BR-09500900 Sao Paulo, Brazil
dc.descriptionUniv Sao Paulo, Dept Biochem &Immunol, Sch Med, BR-09500900 Sao Paulo, Brazil
dc.descriptionState Univ Sao Paulo UNESP, Dept Diag &Surg, Sch Dent Araraquara, BR-14801903 Sao Paulo, Brazil
dc.descriptionCAPES: 3675/07-6
dc.descriptionFAPESP: 05-04247-4
dc.descriptionFAPESP: 05-04351-6
dc.format1-8
dc.languageeng
dc.publisherSpringer
dc.relationInflammation
dc.relation2.884
dc.relation1,023
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectlipopolysaccharide
dc.subjectsignaling pathway
dc.subjectmitogen-activated protein kinases
dc.subjectnuclear factor kappa-light-chain-enhancer of activated B cells
dc.subjectreceptor activator for nuclear factor kappa B ligand
dc.subjectosteoprotegerin
dc.titleRelevance of the Myeloid Differentiation Factor 88 (MyD88) on RANKL, OPG, and Nod Expressions Induced by TLR and IL-1R Signaling in Bone Marrow Stromal Cells
dc.typeArtigo


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