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Upregulation of extracellular matrix metalloproteinase inducer(EMMPRIN) and gelatinase in human atherosclerosis infected with Chlamydia pneumoniae

DC FieldValueLanguage
dc.contributor.author최의영-
dc.contributor.author홍범기-
dc.contributor.author황기철-
dc.contributor.author권혁문-
dc.contributor.author송영구-
dc.date.accessioned2016-05-16T10:52:12Z-
dc.date.available2016-05-16T10:52:12Z-
dc.date.issued2002-
dc.identifier.issn1226-3613-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/143302-
dc.description.abstractChlamydia pneumoniae infection implicated as an important etiologic factor of atherosclerosis, especially in coronary artery disease (CAD), was found in vitro to be associated with the induction of matrix metalloproteinases (MMPs). An extracellular matrix metalloproteinase inducer (EMMPRIN)/ membrane-type 1 matrix metalloproteinase (MT1-MMP) system which induces and activates MMPs, is suggested to be functional and were upregulated in the failing myocardium. However, the upstream regulation of MMPs by C. pneumoniae within atheroma itself remains unclear. We evaluated the seroepidemiologic study of C. pneumoniae infection in CAD patients (n= 391) and controls (n=97) and performed histopathological and in vitro analysis in atherosclerotic vascular tissues obtained from patients with seropositive to C. pneumoniae (n=20), by using immunochemistry for C. pneumoniae, EMMPRIN/MT1-MMP, MMP-2, and MMP-9. The seropositive rates of both anti-C. pneumoniae IgG and IgA were 56.7% in CAD group and 43.3% in control group (P=0.033). Seropositive rate was increased in subgroups of CAD patients without conventional coronary risk factors compared to those with conventional risk factors. Immunoreactivities of EMMPRIN, MT1-MMP, MMP-2, and MMP-9 were increased in the atheromatous plaque itself, predominantly in immunoreactive macrophages/mononuclear cells to C. pneumoniae. Furthermore, Western blot analysis showed that EMMPRIN and MMP-2 were detected more prominently in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. Zymographic analysis revealed that activities of MMP-2 and MMP-9 were more increased in atherosclerotic tissues infected with C. pneumoniae compared to control tissues. The present study demonstrated upstream regulation of MMPs can be induced by C. pneumoniae within atheromatous plaque itself. These findings help to understand the potential role of C. pneumoniae in the progression of atherosclerosis-
dc.description.statementOfResponsibilityopen-
dc.format.extent391~400-
dc.relation.isPartOfEXPERIMENTAL AND MOLECULAR MEDICINE-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAged-
dc.subject.MESHAnimals-
dc.subject.MESHAntigens, CD*-
dc.subject.MESHAntigens, Neoplasm*-
dc.subject.MESHArteriosclerosis/complications-
dc.subject.MESHArteriosclerosis/enzymology-
dc.subject.MESHArteriosclerosis/microbiology*-
dc.subject.MESHArteriosclerosis/pathology*-
dc.subject.MESHBasigin-
dc.subject.MESHBlotting, Western-
dc.subject.MESHChlamydiaInfections/complications*-
dc.subject.MESHChlamydiaInfections/enzymology-
dc.subject.MESHChlamydiaInfections/epidemiology-
dc.subject.MESHChlamydiaInfections/immunology-
dc.subject.MESHChlamydophila pneumoniae/immunology-
dc.subject.MESHChlamydophila pneumoniae/pathogenicity*-
dc.subject.MESHDisease Progression-
dc.subject.MESHExtracellularMatrix/enzymology-
dc.subject.MESHFemale-
dc.subject.MESHGelatinases/metabolism*-
dc.subject.MESHHumans-
dc.subject.MESHImmunohistochemistry-
dc.subject.MESHMale-
dc.subject.MESHMatrixMetalloproteinases/metabolism*-
dc.subject.MESHMembrane Glycoproteins/metabolism*-
dc.subject.MESHMiddle Aged-
dc.subject.MESHUp-Regulation-
dc.titleUpregulation of extracellular matrix metalloproteinase inducer(EMMPRIN) and gelatinase in human atherosclerosis infected with Chlamydia pneumoniae-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Life Science (의생명과학부)-
dc.contributor.googleauthorEui Young Choi-
dc.contributor.googleauthorDongsoo Kim-
dc.contributor.googleauthorBum Kee Hong-
dc.contributor.googleauthorHyuck Moon Kwon-
dc.contributor.googleauthorYoung Goo Song-
dc.contributor.googleauthorKi Hyun Byun-
dc.contributor.googleauthorHyun-Young Park-
dc.contributor.googleauthorKi Chul Whang-
dc.contributor.googleauthorHyun-Seung Kim-
dc.identifier.doi10.1038/emm.2002.56-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA04165-
dc.contributor.localIdA04394-
dc.contributor.localIdA04456-
dc.contributor.localIdA00260-
dc.contributor.localIdA02037-
dc.relation.journalcodeJ00860-
dc.identifier.eissn2092-6413-
dc.identifier.pmid12526080-
dc.subject.keywordarteriosclerosis-
dc.subject.keywordchlamydia-
dc.subject.keywordenzyme induction-
dc.subject.keywordmatrix metalloproteinases-
dc.subject.keywordtissue inhibitor of metalloproteinases-
dc.contributor.alternativeNameChoi, Eui Young-
dc.contributor.alternativeNameHong, Bum Kee-
dc.contributor.alternativeNameHwang, Ki Chul-
dc.contributor.alternativeNameKwon, Hyuck Moon-
dc.contributor.alternativeNameSong, Young Goo-
dc.contributor.affiliatedAuthorChoi, Eui Young-
dc.contributor.affiliatedAuthorHong, Bum Kee-
dc.contributor.affiliatedAuthorHwang, Ki Chul-
dc.contributor.affiliatedAuthorKwon, Hyuck Moon-
dc.contributor.affiliatedAuthorSong, Young Goo-
dc.rights.accessRightsfree-
dc.citation.volume34-
dc.citation.number6-
dc.citation.startPage391-
dc.citation.endPage400-
dc.identifier.bibliographicCitationEXPERIMENTAL AND MOLECULAR MEDICINE, Vol.34(6) : 391-400, 2002-
dc.identifier.rimsid53049-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers

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