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A dominant function of p38 mitogen-activated protein kinase signaling in receptor activator of nuclear factor-κB ligand expression and osteoclastogenesis induction by Aggregatibacter actinomycetemcomitans and Escherichia coli lipopolysaccharide
dc.contributor.authorRossa, Carlosen_US
dc.contributor.authorLiu, M.en_US
dc.contributor.authorKirkwood, Keith L.en_US
dc.date.accessioned2010-04-01T15:18:55Z
dc.date.available2010-04-01T15:18:55Z
dc.date.issued2008-04en_US
dc.identifier.citationRossa, C.; Liu, M.; Kirkwood, K. L. (2008). "A dominant function of p38 mitogen-activated protein kinase signaling in receptor activator of nuclear factor-κB ligand expression and osteoclastogenesis induction by Aggregatibacter actinomycetemcomitans and Escherichia coli lipopolysaccharide." Journal of Periodontal Research 43(2): 201-211. <http://hdl.handle.net/2027.42/65788>en_US
dc.identifier.issn0022-3484en_US
dc.identifier.issn1600-0765en_US
dc.identifier.urihttps://hdl.handle.net/2027.42/65788
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/sites/entrez?cmd=retrieve&db=pubmed&list_uids=18302623&dopt=citationen_US
dc.description.abstractLipopolysaccharide from gram-negative bacteria is one of the microbial-associated molecular patterns that initiate the immune/inflammatory response, leading to the tissue destruction observed in periodontitis. The aim of this study was to evaluate the role of the p38 mitogen-activated protein kinase (MAPK) signaling pathway in lipopolysaccharide-induced receptor activator of nuclear factor-κB ligand (RANKL) expression by murine periodontal ligament cells. Material and Methods:  Expression of RANKL and osteoprotegerin mRNA was studied by reverse transcription-polymerase chain reaction upon stimulation with lipopolysaccharide from Escherichia coli and Aggregatibacter actinomycetemcomitans . The biochemical inhibitor SB203580 was used to evaluate the contribution of the p38 MAPK signaling pathway to lipopolysaccharide-induced RANKL and osteoprotegerin expression. Stable cell lines expressing dominant-negative forms of MAPK kinase (MKK)-3 and MKK6 were generated to confirm the role of the p38 MAPK pathway. An osteoclastogenesis assay using a coculture model of the murine monocytic cell line RAW 264.7 was used to determine if osteoclast differentiation induced by lipopolysaccharide-stimulated periodontal ligament was correlated with RANKL expression. Results:  Inhibiting p38 MAPK prior to lipopolysaccharide stimulation resulted in a significant decrease of RANKL mRNA expression. Osteoprotegerin mRNA expression was not affected by lipopolysaccharide or p38 MAPK. Lipopolysaccharide-stimulated periodontal ligament cells increased osteoclast differentiation, an effect that was completely blocked by osteoprotegerin and significantly decreased by inhibition of MKK3 and MKK6, upstream activators of p38 MAPK. Conditioned medium from murine periodontal ligament cultures did not increase osteoclast differentiation, indicating that periodontal ligament cells produced membrane-bound RANKL. Conclusion:  Lipopolysaccharide resulted in a significant increase of RANKL in periodontal ligament cells. The p38 MAPK pathway is required for lipopolysaccharide-induced membrane-bound RANKL expression in these cells.en_US
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dc.format.mimetypeapplication/pdf
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dc.publisherBlackwell Publishing Ltden_US
dc.rightsJournal compilation © 2008 Blackwell Munksgaarden_US
dc.subject.otherosteoclastogenesisen_US
dc.subject.otherp38 mitogen-activated protein kinaseen_US
dc.subject.otherperiodontal ligament cellsen_US
dc.subject.otherreceptor activator of nuclear factor-ΚB liganden_US
dc.titleA dominant function of p38 mitogen-activated protein kinase signaling in receptor activator of nuclear factor-κB ligand expression and osteoclastogenesis induction by Aggregatibacter actinomycetemcomitans and Escherichia coli lipopolysaccharideen_US
dc.typeArticleen_US
dc.rights.robotsIndexNoFollowen_US
dc.subject.hlbsecondlevelDentistryen_US
dc.subject.hlbtoplevelHealth Sciencesen_US
dc.description.peerreviewedPeer Revieweden_US
dc.contributor.affiliationumDepartment of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI, USAen_US
dc.contributor.affiliationotherDepartment of Diagnosis and Surgery, School of Dentistry at Araraquara, State University of Sao Paulo (UNESP), Araraquara, SP, Brazilen_US
dc.identifier.pmid18302623en_US
dc.description.bitstreamurlhttp://deepblue.lib.umich.edu/bitstream/2027.42/65788/1/j.1600-0765.2007.01013.x.pdf
dc.identifier.doi10.1111/j.1600-0765.2007.01013.xen_US
dc.identifier.sourceJournal of Periodontal Researchen_US
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dc.owningcollnameInterdisciplinary and Peer-Reviewed


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