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Article: Induction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki disease

TitleInduction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki disease
Authors
Issue Date2005
PublisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/
Citation
Pediatric Research, 2005, v. 58 n. 6, p. 1306-1310 How to Cite?
Abstract
Evidence of premature atherosclerosis late after Kawasaki disease (KD) is accumulating. Given the potential roles of monocyte chemoattractant protein-1 (MCP-1), chemokine receptor CCR-2, and inducible nitric oxide synthase (iNOS) in atherogenesis, we sought to determine whether serum obtained from children late after KD would induce expression of these genes in macrophages in vitro. A total of 79 subjects were studied, which comprised 57 KD patients, 33 of whom had coronary aneurysms, and 22 age-matched controls. Expression of MCP-1, CCR2, and iNOS mRNA in THP-1 macrophages in the presence of patient and control serum was quantified as a ratio to β-actin mRNA and expressed as a percentage of control. MCP-1 expression was significantly increased in the presence of serum from patients with coronary aneurysms. Expression of CCR2 and iNOS was significantly increased when THP-1 macrophages were incubated with serum from patients with and without coronary aneurysms. The magnitude of induction of MCP-1, CCR2, and iNOS or in combinations correlated positively with serum high-sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) cholesterol levels and negatively with high-density lipoprotein (HDL) cholesterol level. In conclusion, the serum of patients with a history of KD induces expression of MCP-1, CCR2, and iNOS in THP-1 macrophages in vitro. Induction of these genes in vivo may be related to chronic inflammation and may have important implications for premature atherosclerosis. Copyright © 2005 International Pediatric Research Foundation, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/170352
ISSN
2013 Impact Factor: 2.840
ISI Accession Number ID
References

 

Author Affiliations
  1. University of Manitoba
  2. The University of Hong Kong
  3. Queen Mary Hospital Hong Kong
DC FieldValueLanguage
dc.contributor.authorCheung, YFen_US
dc.contributor.authorKarmin, Oen_US
dc.contributor.authorTam, SCFen_US
dc.contributor.authorSiow, YLen_US
dc.date.accessioned2012-10-30T06:07:44Z-
dc.date.available2012-10-30T06:07:44Z-
dc.date.issued2005en_US
dc.identifier.citationPediatric Research, 2005, v. 58 n. 6, p. 1306-1310en_US
dc.identifier.issn0031-3998en_US
dc.identifier.urihttp://hdl.handle.net/10722/170352-
dc.description.abstractEvidence of premature atherosclerosis late after Kawasaki disease (KD) is accumulating. Given the potential roles of monocyte chemoattractant protein-1 (MCP-1), chemokine receptor CCR-2, and inducible nitric oxide synthase (iNOS) in atherogenesis, we sought to determine whether serum obtained from children late after KD would induce expression of these genes in macrophages in vitro. A total of 79 subjects were studied, which comprised 57 KD patients, 33 of whom had coronary aneurysms, and 22 age-matched controls. Expression of MCP-1, CCR2, and iNOS mRNA in THP-1 macrophages in the presence of patient and control serum was quantified as a ratio to β-actin mRNA and expressed as a percentage of control. MCP-1 expression was significantly increased in the presence of serum from patients with coronary aneurysms. Expression of CCR2 and iNOS was significantly increased when THP-1 macrophages were incubated with serum from patients with and without coronary aneurysms. The magnitude of induction of MCP-1, CCR2, and iNOS or in combinations correlated positively with serum high-sensitivity C-reactive protein (hs-CRP), and low-density lipoprotein (LDL) cholesterol levels and negatively with high-density lipoprotein (HDL) cholesterol level. In conclusion, the serum of patients with a history of KD induces expression of MCP-1, CCR2, and iNOS in THP-1 macrophages in vitro. Induction of these genes in vivo may be related to chronic inflammation and may have important implications for premature atherosclerosis. Copyright © 2005 International Pediatric Research Foundation, Inc.en_US
dc.languageengen_US
dc.publisherLippincott Williams & Wilkins. The Journal's web site is located at http://www.pedresearch.org/en_US
dc.relation.ispartofPediatric Researchen_US
dc.subject.meshAtherosclerosis - Geneticsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshChemokine Ccl2 - Geneticsen_US
dc.subject.meshChilden_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expressionen_US
dc.subject.meshHumansen_US
dc.subject.meshLipids - Blooden_US
dc.subject.meshMacrophages - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMucocutaneous Lymph Node Syndrome - Complications - Genetics - Immunologyen_US
dc.subject.meshNitric Oxide Synthase Type Ii - Geneticsen_US
dc.subject.meshReceptors, Ccr2en_US
dc.subject.meshReceptors, Chemokine - Geneticsen_US
dc.subject.meshSerum - Metabolismen_US
dc.subject.meshUp-Regulation - Geneticsen_US
dc.titleInduction of MCP1, CCR2, and iNOS expression in THP-1 macrophages by serum of children late after kawasaki diseaseen_US
dc.typeArticleen_US
dc.identifier.emailCheung, YF:xfcheung@hku.hken_US
dc.identifier.authorityCheung, YF=rp00382en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1203/01.pdr.0000183360.79872.1cen_US
dc.identifier.pmid16306213en_US
dc.identifier.scopuseid_2-s2.0-27644468219en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-27644468219&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume58en_US
dc.identifier.issue6en_US
dc.identifier.spage1306en_US
dc.identifier.epage1310en_US
dc.identifier.isiWOS:000233416500031-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridCheung, YF=7202111067en_US
dc.identifier.scopusauthoridKarmin, O=6604083266en_US
dc.identifier.scopusauthoridTam, SCF=7202037323en_US
dc.identifier.scopusauthoridSiow, YL=7003336463en_US

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