Atherosclerosis

2004

DOI: 10.1016/j.atherosclerosis.2004.01.009

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Rosuvastatin reduces MMP-7 secretion by human monocyte-derived macrophages: potential relevance to atherosclerotic plaque stability

Christophe Furman

¹

,

²

,

Mejid Kandoussi

³

et al.

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Discussion1

Effect Of Statins On Cac1

Specific and Dose-dependent Binding Of Mmp-7 To Connexin-431

Clinical Perspective P 29281

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Cited by 84 publications

(55 citation statements)

References 45 publications

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“…Statins have been shown to alter the production of various MMPs both in vivo and in vitro (32)(33)(34), and it is likely that statin medication could have also influenced plasma concentrations of MMPs and TIMP-1 in the present study. In their study, Furman et al (34 ) demonstrated that rosuvastatin decreases the secretion of MMP-7 from human macrophages in vitro.…”

Section: Discussionmentioning

confidence: 77%

Increased Plasma Concentration of Matrix Metalloproteinase-7 in Patients with Coronary Artery Disease

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et al. 2006

Clinical Chemistry

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Background: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers. Methods: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method. Results: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively

“…Statins have been shown to alter the production of various MMPs both in vivo and in vitro (32)(33)(34), and it is likely that statin medication could have also influenced plasma concentrations of MMPs and TIMP-1 in the present study. In their study, Furman et al (34 ) demonstrated that rosuvastatin decreases the secretion of MMP-7 from human macrophages in vitro.…”

Section: Discussionmentioning

confidence: 77%

Increased Plasma Concentration of Matrix Metalloproteinase-7 in Patients with Coronary Artery Disease

¹

,

²

,

et al. 2006

Clinical Chemistry

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Background: Plaque rupture is often associated with breakdown of the extracellular matrix in the shoulder region of a plaque. We tested whether plasma concentrations of various matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinase-1 (TIMP-1) could serve as markers for plaque instability as well as relationships between plasma MMPs and inflammatory markers. Methods: The study group included 65 men with angiographically verified CAD (45 with stable and 20 with unstable CAD) and 28 healthy controls. Circulating MMP, TIMP-1, C-reactive protein, and cytokine concentrations were measured by ELISA. Leukocyte subtype counts in whole blood were determined, and T-cell subsets and natural killer cells were measured by flow cytometry. Differences in continuous variables between groups were tested by ANOVA with the Scheffé F-test used as a post hoc test, and correlations were analyzed by a linear regression method. Results: The plasma concentration of MMP-7 was increased in patients with stable and unstable CAD, whereas MMP-2 and -3 concentrations were decreased. The plasma concentration of TIMP-1 was significantly increased in patients with unstable CAD. MMP-2, -3, and -7 showed no correlations with established markers of inflammation. However, MMP-2 correlated positively

“…The observed plaque stabilization effect induced by statins might potentially be attributed to pleomorphic effect including a decrease in the lipid content of plaques, a reduction in the inflammatory burden and an improvement in endothelial function; all promoting a more stable phenotype (67)(68)(69)(70)(71). Notwithstanding, most evidence in this regard remains inconclusive or speculative.…”

Section: Effect Of Statins On Cacmentioning

confidence: 89%

Progression of coronary artery calcification at the crossroads: sign of progression or stabilization of coronary atherosclerosis?

Rodríguez-Granillo

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,

²

,

³

2016

Cardiovasc. Diagn. Ther.

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Coronary artery calcification (CAC) has been strongly established as an independent predictor of adverse events, with a significant incremental prognostic value over traditional risk stratification algorithms.CAC progression has been associated with a higher rate of events. In parallel, several randomized studies and meta-analysis have shown the effectiveness of statins to slow progression and even promote plaque regression. However, evidence regarding the effect of routine medical therapy on CAC has yielded conflicting results, with initial studies showing significant CAC regression, and contemporaneous data showing rather the opposite. Accordingly, there is currently a great controversy on whether progression of CAC is a sign of progression or stabilization of coronary artery disease (CAD). The finding of inexorable CAC progression despite the implementation of intensive contemporaneous medical therapy suggests that further understanding of this phenomenon should be undertaken before the implementation of CAC as a surrogate endpoint for longitudinal studies, or for prospective follow-up of patients under routine medical treatment.

“…The classic protein association phase (black line in Figure 4B) occurred during the MMP-7 pulse and was followed by dissociation during the buffer only injection. The on rate (k a ), determined by dose-response curves, was 1.5ϫ10 4 (1/ms), indicating high specificity and affinity of MMP-7 binding to connexin-43.…”

Section: Specific and Dose-dependent Binding Of Mmp-7 To Connexin-43mentioning

confidence: 99%

“…MMP-7 is expressed in macrophages 4,5 and cardiomyocytes 6 after MI. Pro-MMP-7 is 28 kDa; active-MMP-7 is 19 kDa.…”

Section: Clinical Perspective P 2928mentioning

confidence: 99%

Matrix Metalloproteinase-7 Affects Connexin-43 Levels, Electrical Conduction, and Survival After Myocardial Infarction

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et al. 2006

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Background-Matrix metalloproteinases (MMPs) contribute to left ventricular remodeling after myocardial infarction (MI). Specific causative roles of particular MMPs, however, remain unclear. MMP-7 is abundant in cardiomyocytes and macrophages, but MMP-7 function after MI has not been defined. Methods and Results-Wild-type (WT; nϭ55) and MMP-7-null (MMP-7 Ϫ/Ϫ ; nϭ32) mice underwent permanent coronary artery ligation for 7 days. MI sizes were similar, but survival was greatly improved in MMP-7 Ϫ/Ϫ mice. The survival difference could not be attributed to differences in left ventricular dilation because end-diastolic volumes increased similarly. ECG analysis revealed a prolonged PR interval in WT but not in MMP-7 Ϫ/Ϫ post-MI mice. Post-MI conduction velocity, determined by optically mapping electrical wavefront propagation, decreased to 78Ϯ6% of control for WT and was normalized in MMP-7 Ϫ/Ϫ mice. In WT mice, slower conduction velocity correlated with a 53% reduction in the gap junction protein connexin-43. Direct binding of MMP-7 to connexin-43, determined by surface plasmon resonance technology, occurred in a dose-dependent manner. Connexin-43 processing by MMP-7 was confirmed by in silico and in vitro substrate analyses and MMP-7 infusion induced arrhythmias in vivo. Conclusions-MMP-7 deletion results in improved survival and myocardial conduction patterns after MI. This is the first report to implicate MMP-7 in post-MI remodeling and to demonstrate that connexin-43 is a novel MMP-7 substrate.

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