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Metalloproteinases-2, -9 and TIMP-1 expression in stable and unstable coronary plaques undergoing PCI.

FIOTTI, NICOLA
•
ALTAMURA N
•
ORLANDO C
altro
GIANSANTE, CARLO
2008
  • journal article

Periodico
INTERNATIONAL JOURNAL OF CARDIOLOGY
Abstract
Introduction: Experimental models and ex-vivo studies suggest a crucial role of some matrix metalloproteinases (MMPs) in the development of acute coronary syndromes, but expression levels of MMP-2, MMP-9 and TIMP-1 in human coronary plaques causing stable angina or an acute coronary syndrome have not been reported, yet. Methods: MMP-2, -9 and TIMP-1 expressions were assessed by real-time PCR from the debris collected into distal protective vascular guards from patients with stable angina (SA-Group, n=16), acute coronary syndrome (ACS-Group, n=16) undergoing percutaneous coronary interventions (PCI). MMP-2 and -9 activities were also evaluated by gelatin-substrate zymography on plasma samples collected immediately before PCI, and compared to those of healthy subjects (Control-Group). Results: The expression of MMP-2 was similar in ACS and SA-Groups. MMP-9 (P=0.011), but not TIMP-1, expression was higher in debris samples from patients in the ACS-Group than in SA-Group. In both groups, the expression of MMP-2 and MMP-9 were inversely correlated (rho=−0.7; Pb0.004). Zymography data indicated that pro and active MMP-9 were higher in ACS than in SA-Group, while no difference in MMP-2 was found. Conclusions: MMP-9, but not TIMP-1 or MMP-2 expression is increased in plaques causing acute coronary syndrome.
DOI
10.1016/J.IJCARD.2007.05.011
WOS
WOS:000257205500009
Archivio
http://hdl.handle.net/11368/1709111
info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-45849118027
Diritti
metadata only access
Soggetti
  • Gene Expression

  • primary percutaneous ...

  • matrix metalloprotein...

  • acute coronary syndro...

  • Atherosclerosis

Scopus© citazioni
38
Data di acquisizione
Jun 14, 2022
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Web of Science© citazioni
36
Data di acquisizione
Mar 26, 2024
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Data di acquisizione
Apr 19, 2024
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