scholarly journals Upregulation of extracellular matrix metalloproteinase inducer (EMMPRIN) and gelatinases in human atherosclerosis infected with Chlamydia pneumoniae: The potential role of Chlamydia pneumoniae infection in the progression of atherosclerosis

2002 ◽  
Vol 34 (6) ◽  
pp. 391-400 ◽  
Author(s):  
Eui Young Choi ◽  
Dongsoo Kim ◽  
Bum Kee Hong ◽  
Hyuck Moon Kwon ◽  
Young Goo Song ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Potential Role ◽  
Chlamydia Pneumoniae ◽  
Extracellular Matrix Metalloproteinase Inducer ◽  
Human Atherosclerosis ◽  
Progression Of Atherosclerosis

The role of extracellular matrix metalloproteinase inducer protein in prostate cancer progression

2008 ◽  
Vol 57 (9) ◽  
pp. 1367-1379 ◽  
Author(s):  
Michele C. Madigan ◽  
Elizabeth A. Kingsley ◽  
Paul J. Cozzi ◽  
Warick J. Delprado ◽  
Pamela J. Russell ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Cancer Progression ◽  
Prostate Cancer Progression ◽  
Extracellular Matrix Metalloproteinase Inducer

EMMPRIN (CD 147) is a central activator of extracellular matrix degradation by Chlamydia pneumoniae-infected monocytes.

2006 ◽  
Vol 95 (01) ◽  
pp. 151-158 ◽  
Author(s):  
Roland Schmidt ◽  
Vanessa Redecke ◽  
Yoshi Breitfeld ◽  
Nina Wantia ◽  
Thomas Miethke ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Matrix Metalloproteinase ◽  
Chlamydia Pneumoniae ◽  
Surface Expression ◽  
Heat Shock Protein 60 ◽  
Membrane Type ◽  
Activation Pathways ◽  
Accelerate Atherosclerosis

Summary Chlamydia (C.) pneumoniae are thought to infect monocytes and use them as vectors into the vessel wall, where they may accelerate atherosclerosis. We investigated the effects of C. pneumoniae on monocytic matrix metalloproteinase (MMP) activation with focus on the role of the extracellular matrix metalloproteinase inducer EMMPRIN. Human monocytes or monocytic MonoMac6 cells were infected with C. pneumoniae. Infection enhanced mRNA-and surface expression of EMMPRIN and Membrane-type-1 Matrix Metalloproteinase (MT1-MMP), plus the secretion of MMP-7, MMP-9 and the urokinase receptor (uPAR). Chlamydial heat shock protein 60 was identified to be partially responsible for EMMPRIN and MMP-9 induction, while C. trachomatis-infection had no stimulatory effect, indicatinga C. pneumoniae-specific activation pathway. Suppression of EMMPRIN by gene silencing almost completely hindered the induction of MT1-MMP and MMP-9 by C. pneumoniae, suggesting a predominant regulatory role for EMMPRIN. Moreover, C. pneumoniae-infected monocytes exhibited increased MMP-and plasmin-dependent migration through “matrigel”. Additionally, incubation of SMCs with supernatants of C. pneumoniae-infected monocytes induced MMP-2 activation, which was inhibited by IL1-Receptor antagonist or anti-IL-6-mAb, indicating paracrine intercellular activation pathways. In conclusion,C. pneumoniae induce MMP activity directly in monocytes through an EMMPRINdependent pathway and indirectly in SMCs via monocytederived cytokines.

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