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

Authors
 Eui Young Choi  ;  Dongsoo Kim  ;  Bum Kee Hong  ;  Hyuck Moon Kwon  ;  Young Goo Song  ;  Ki Hyun Byun  ;  Hyun-Young Park  ;  Ki Chul Whang  ;  Hyun-Seung Kim 
Citation
 EXPERIMENTAL AND MOLECULAR MEDICINE, Vol.34(6) : 391-400, 2002 
Journal Title
EXPERIMENTAL AND MOLECULAR MEDICINE
ISSN
 1226-3613 
Issue Date
2002
MeSH
Aged ; Animals ; Antigens, CD* ; Antigens, Neoplasm* ; Arteriosclerosis/complications ; Arteriosclerosis/enzymology ; Arteriosclerosis/microbiology* ; Arteriosclerosis/pathology* ; Basigin ; Blotting, Western ; ChlamydiaInfections/complications* ; ChlamydiaInfections/enzymology ; ChlamydiaInfections/epidemiology ; ChlamydiaInfections/immunology ; Chlamydophila pneumoniae/immunology ; Chlamydophila pneumoniae/pathogenicity* ; Disease Progression ; ExtracellularMatrix/enzymology ; Female ; Gelatinases/metabolism* ; Humans ; Immunohistochemistry ; Male ; MatrixMetalloproteinases/metabolism* ; Membrane Glycoproteins/metabolism* ; Middle Aged ; Up-Regulation
Keywords
arteriosclerosis ; chlamydia ; enzyme induction ; matrix metalloproteinases ; tissue inhibitor of metalloproteinases
Abstract
Chlamydia 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
Files in This Item:
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DOI
10.1038/emm.2002.56
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
Yonsei Authors
Kwon, Hyuck Moon(권혁문) ORCID logo https://orcid.org/0000-0001-9901-5015
Song, Young Goo(송영구) ORCID logo https://orcid.org/0000-0002-0733-4156
Choi, Eui Young(최의영) ORCID logo https://orcid.org/0000-0003-3732-0190
Hong, Bum Kee(홍범기) ORCID logo https://orcid.org/0000-0002-6456-0184
Hwang, Ki Chul(황기철)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/143302
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