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Article: A novel pathophysiological mechanism for osteoporosis suggested by an in vivo gene expression study of circulating monocytes

TitleA novel pathophysiological mechanism for osteoporosis suggested by an in vivo gene expression study of circulating monocytes
Authors
Issue Date2005
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2005, v. 280 n. 32, p. 29011-29016 How to Cite?
AbstractBone mineral density (BMD) is a major risk factor for osteoporosis. Circulating monocytes may serve as early progenitors of osteoclasts and produce a wide variety of factors important to bone metabolism. However, little is known about the roles of circulating monocytes in relation to the pathophysiology of osteoporosis. Using the Affymetrix HG-U133A GeneChip® array, we performed a comparative gene expression study of circulating monocytes in subjects with high and low BMD. We identified in total 66 differentially expressed genes including some novel as well as some already known to be relevant to bone metabolism. Three genes potentially contributing to bone metabolism, CCR3 (chemokine receptor 3), HDC (histidine decarboxylase, i.e. the histamine synthesis enzyme), and GCA (glucocorticoid receptor), were confirmed by quantitative real-time reverse transcriptase-PCR as up-regulated in subjects with lower BMD. In addition, significant negative correlation was observed between expression levels of the genes and BMD Z-scores. These three genes and/or their products mediate monocyte chemotaxis, histamine production, and/or sensitivity to glucocorticoids. Our results suggest a novel pathophysiological mechanism for osteoporosis that is characterized by increased recruitment of circulating monocyte into bone, enhanced monocyte differentiation into osteoclasts, as well as osteoclast stimulation via monocyte functional changes. This is the first in vivo microarray study of osteoporosis in humans. The results may contribute to identification of new genes and their functions for osteoporosis and suggest genetic markers to discern individuals at higher risk to osteoporosis with an aim for preventive intervention and treatment. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/178897
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, YZen_US
dc.contributor.authorDvornyk, Ven_US
dc.contributor.authorLu, Yen_US
dc.contributor.authorShen, Hen_US
dc.contributor.authorLappe, JMen_US
dc.contributor.authorRecker, RRen_US
dc.contributor.authorDeng, HWen_US
dc.date.accessioned2012-12-19T09:50:32Z-
dc.date.available2012-12-19T09:50:32Z-
dc.date.issued2005en_US
dc.identifier.citationJournal Of Biological Chemistry, 2005, v. 280 n. 32, p. 29011-29016en_US
dc.identifier.issn0021-9258en_US
dc.identifier.urihttp://hdl.handle.net/10722/178897-
dc.description.abstractBone mineral density (BMD) is a major risk factor for osteoporosis. Circulating monocytes may serve as early progenitors of osteoclasts and produce a wide variety of factors important to bone metabolism. However, little is known about the roles of circulating monocytes in relation to the pathophysiology of osteoporosis. Using the Affymetrix HG-U133A GeneChip® array, we performed a comparative gene expression study of circulating monocytes in subjects with high and low BMD. We identified in total 66 differentially expressed genes including some novel as well as some already known to be relevant to bone metabolism. Three genes potentially contributing to bone metabolism, CCR3 (chemokine receptor 3), HDC (histidine decarboxylase, i.e. the histamine synthesis enzyme), and GCA (glucocorticoid receptor), were confirmed by quantitative real-time reverse transcriptase-PCR as up-regulated in subjects with lower BMD. In addition, significant negative correlation was observed between expression levels of the genes and BMD Z-scores. These three genes and/or their products mediate monocyte chemotaxis, histamine production, and/or sensitivity to glucocorticoids. Our results suggest a novel pathophysiological mechanism for osteoporosis that is characterized by increased recruitment of circulating monocyte into bone, enhanced monocyte differentiation into osteoclasts, as well as osteoclast stimulation via monocyte functional changes. This is the first in vivo microarray study of osteoporosis in humans. The results may contribute to identification of new genes and their functions for osteoporosis and suggest genetic markers to discern individuals at higher risk to osteoporosis with an aim for preventive intervention and treatment. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.en_US
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_US
dc.relation.ispartofJournal of Biological Chemistryen_US
dc.subject.meshAgeden_US
dc.subject.meshAlgorithmsen_US
dc.subject.meshBone Densityen_US
dc.subject.meshChemotaxisen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshGlucocorticoids - Metabolismen_US
dc.subject.meshHistidine Decarboxylase - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshLumbar Vertebrae - Metabolismen_US
dc.subject.meshMiddle Ageden_US
dc.subject.meshModels, Biologicalen_US
dc.subject.meshMonocytes - Cytology - Metabolismen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshOsteoporosis - Blood - Genetics - Pathologyen_US
dc.subject.meshReceptors, Ccr3en_US
dc.subject.meshReceptors, Chemokine - Metabolismen_US
dc.subject.meshReceptors, Glucocorticoid - Metabolismen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshRisk Factorsen_US
dc.titleA novel pathophysiological mechanism for osteoporosis suggested by an in vivo gene expression study of circulating monocytesen_US
dc.typeArticleen_US
dc.identifier.emailDvornyk, V: dvornyk@hku.hken_US
dc.identifier.authorityDvornyk, V=rp00693en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M501164200en_US
dc.identifier.pmid15965235-
dc.identifier.scopuseid_2-s2.0-23844495088en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-23844495088&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume280en_US
dc.identifier.issue32en_US
dc.identifier.spage29011en_US
dc.identifier.epage29016en_US
dc.identifier.isiWOS:000231021300024-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLiu, YZ=7410227746en_US
dc.identifier.scopusauthoridDvornyk, V=6701789786en_US
dc.identifier.scopusauthoridLu, Y=26321148700en_US
dc.identifier.scopusauthoridShen, H=36126870600en_US
dc.identifier.scopusauthoridLappe, JM=7003431855en_US
dc.identifier.scopusauthoridRecker, RR=7007086875en_US
dc.identifier.scopusauthoridDeng, HW=34568563000en_US

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