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Article: Cyclic ADP-ribose is a second messenger in the lipopolysaccharide- stimulated proliferation of human peripheral blood mononuclear cells

TitleCyclic ADP-ribose is a second messenger in the lipopolysaccharide- stimulated proliferation of human peripheral blood mononuclear cells
Authors
KeywordsADP-ribosyl cyclase
Cyclic ADP-ribose
Cyclic ADP-ribose hydrolase
Lipopolysaccharide
Nicotinamide-adenine dinucleotide (NAD+)
Peripheral blood mononuclear cell
Issue Date2003
PublisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.org
Citation
Biochemical Journal, 2003, v. 375 n. 2, p. 395-403 How to Cite?
AbstractCyclic ADP-ribose (cADPR), a universal calcium mobilizer from intracellular stores, was recently demonstrated to stimulate proliferation of various cell types. The role of cADPR in a specific process of monocyte- and plasma-mediated activation of T-lymphocytes by lipopolysaccharide (LPS) was addressed using human mononuclear cells from peripheral blood (PBMCs). Incubation of PBMCs with 0.1 μg/ml of LPS for 24 h provided a doubling in the intracellular levels of cADPR as compared with unstimulated PBMCs. The cADPR increase was abolished either by prior removal of monocytes or by pre-incubating a whole PBMC population with a monoclonal antibody against the monocyte marker CD14. The increased concentrations of intracellular cADPR elicited by LPS stimulation were paralleled by significant increases in NAD + levels and in the activities of ectocellular and membrane-bound fractions of ADP-ribosyl cyclase/ cADPR hydrolase activities. A cytosolic ADP-ribosyl cyclase was also detectable in PBMCs and its activity was comparably enhanced by LPS stimulation. This soluble cyclase is distinguished from the membrane-bound cyclase by both substrate and inhibitor sensitivities. LPS-stimulated PBMCs showed 2-3-fold increases of intracellular calcium ([Ca2+]), and these changes were prevented completely by the cADPR antagonist 8-Br-cADPR and by ryanodine. Both compounds, and the cyclase inhibitor nicotinamide, significantly inhibited the T-lymphocyte proliferation induced by LPS in PBMCs. These results demonstrate that cADPR plays a role of second messenger in the adaptive immune recognition process of LPS-stimulated proliferation of PBMCs.
Persistent Identifierhttp://hdl.handle.net/10722/132561
ISSN
2015 Impact Factor: 3.562
2015 SCImago Journal Rankings: 2.582
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorBruzzone, Sen_HK
dc.contributor.authorDe Flora, Aen_HK
dc.contributor.authorUsai, Cen_HK
dc.contributor.authorGraeff, Ren_HK
dc.contributor.authorLee, HCen_HK
dc.date.accessioned2011-03-28T09:26:19Z-
dc.date.available2011-03-28T09:26:19Z-
dc.date.issued2003en_HK
dc.identifier.citationBiochemical Journal, 2003, v. 375 n. 2, p. 395-403en_HK
dc.identifier.issn0264-6021en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132561-
dc.description.abstractCyclic ADP-ribose (cADPR), a universal calcium mobilizer from intracellular stores, was recently demonstrated to stimulate proliferation of various cell types. The role of cADPR in a specific process of monocyte- and plasma-mediated activation of T-lymphocytes by lipopolysaccharide (LPS) was addressed using human mononuclear cells from peripheral blood (PBMCs). Incubation of PBMCs with 0.1 μg/ml of LPS for 24 h provided a doubling in the intracellular levels of cADPR as compared with unstimulated PBMCs. The cADPR increase was abolished either by prior removal of monocytes or by pre-incubating a whole PBMC population with a monoclonal antibody against the monocyte marker CD14. The increased concentrations of intracellular cADPR elicited by LPS stimulation were paralleled by significant increases in NAD + levels and in the activities of ectocellular and membrane-bound fractions of ADP-ribosyl cyclase/ cADPR hydrolase activities. A cytosolic ADP-ribosyl cyclase was also detectable in PBMCs and its activity was comparably enhanced by LPS stimulation. This soluble cyclase is distinguished from the membrane-bound cyclase by both substrate and inhibitor sensitivities. LPS-stimulated PBMCs showed 2-3-fold increases of intracellular calcium ([Ca2+]), and these changes were prevented completely by the cADPR antagonist 8-Br-cADPR and by ryanodine. Both compounds, and the cyclase inhibitor nicotinamide, significantly inhibited the T-lymphocyte proliferation induced by LPS in PBMCs. These results demonstrate that cADPR plays a role of second messenger in the adaptive immune recognition process of LPS-stimulated proliferation of PBMCs.en_HK
dc.languageengen_US
dc.publisherPortland Press Ltd. The Journal's web site is located at http://www.biochemj.orgen_HK
dc.relation.ispartofBiochemical Journalen_HK
dc.subjectADP-ribosyl cyclaseen_HK
dc.subjectCyclic ADP-riboseen_HK
dc.subjectCyclic ADP-ribose hydrolaseen_HK
dc.subjectLipopolysaccharideen_HK
dc.subjectNicotinamide-adenine dinucleotide (NAD+)en_HK
dc.subjectPeripheral blood mononuclear cellen_HK
dc.titleCyclic ADP-ribose is a second messenger in the lipopolysaccharide- stimulated proliferation of human peripheral blood mononuclear cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailGraeff, R: graeffr@hku.hken_HK
dc.identifier.emailLee, HC: leehc@hku.hken_HK
dc.identifier.authorityGraeff, R=rp01464en_HK
dc.identifier.authorityLee, HC=rp00545en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1042/BJ20030556en_HK
dc.identifier.pmid12852785-
dc.identifier.pmcidPMC1223684-
dc.identifier.scopuseid_2-s2.0-0142169532en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0142169532&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume375en_HK
dc.identifier.issue2en_HK
dc.identifier.spage395en_HK
dc.identifier.epage403en_HK
dc.identifier.isiWOS:000186096400017-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridBruzzone, S=7004633756en_HK
dc.identifier.scopusauthoridDe Flora, A=7006450815en_HK
dc.identifier.scopusauthoridUsai, C=7003897893en_HK
dc.identifier.scopusauthoridGraeff, R=7003614053en_HK
dc.identifier.scopusauthoridLee, HC=26642959100en_HK

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