C-reactive protein induces expression of matrix metalloproteinase-9: A possible link between inflammation and plaque rupture

Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exer...

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Vydané v:	International journal of cardiology Ročník 168; číslo 2; s. 981 - 986
Hlavní autori:	Cimmino, Giovanni, Ragni, Massimo, Cirillo, Plinio, Petrillo, Gianluca, Loffredo, Francesco, Chiariello, Massimo, Gresele, Paolo, Falcinelli, Emanuela, Golino, Paolo
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	Shannon Elsevier Ireland Ltd 30.09.2013 Elsevier
Predmet:	Acute Coronary Syndrome - enzymology Acute Coronary Syndrome - genetics Acute Coronary Syndrome - metabolism Acute coronary syndromes Aged Biological and medical sciences C-Reactive Protein - metabolism C-Reactive Protein - physiology Cardiology. Vascular system Cardiovascular Cells, Cultured Coronary heart disease CRP Female Gene Expression Regulation, Enzymologic Heart Humans Inflammation - enzymology Inflammation - genetics Inflammation - metabolism Male Matrix Metalloproteinase 9 - biosynthesis Matrix Metalloproteinase 9 - genetics Medical sciences Middle Aged MMP-9 Muscle, Smooth, Vascular - enzymology Muscle, Smooth, Vascular - metabolism Myocarditis. Cardiomyopathies Myocytes, Smooth Muscle - enzymology Myocytes, Smooth Muscle - pathology Plaque, Atherosclerotic - blood Plaque, Atherosclerotic - enzymology Plaque, Atherosclerotic - metabolism Up-Regulation - genetics CRP Acute coronary syndromes MMP-9 Enzyme Rupture Metalloendopeptidases Cardiovascular disease Inflammation Gene expression Coronary heart disease Myocardial disease Gelatinase B Peptidases Acute phase protein Hydrolases Cardiology C reactive protein Acute coronary syndrome
ISSN:	0167-5273, 1874-1754, 1874-1754
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Abstract	Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exert direct pro-atherosclerotic effects. Therefore, we aimed at determining whether CRP might induce MMP-9 in two different experimental conditions: 1) smooth muscle cells (SMCs) in vitro, and 2) patients with ACS. Effects of increasing concentrations of CRP on MMP-9 expression were evaluated in vitro in human SMCs. TIMP-1 protein expression, the selective inhibitor of MMP-9, was also evaluated. CRP dose-dependently induced MMP-9 expression in SMCs by promoting MMP-mRNA transcription, as well as MMP-9 secretion. In contrast, no differences were found for TIMP-1 protein expression. In vivo, MMP-9 and CRP levels were measured in blood samples obtained from the aorta (Ao) and the coronary sinus (Cs) of patients with normal coronary arteries (controls, n=21), stable angina (n=24), and ACS (n=30). Both MMP-9 and CRP plasma levels were significantly increased across the coronary circulation only in patients with ACS. Interestingly, a significant correlation between MMP-9 and CRP plasma levels was found. CRP induced MMP-9 expression and activity in human SMCs in culture; patients presenting with ACS have increased transcoronary plasma levels of MMP-9 and CRP with a significant correlation between these two markers. This may explain the heightened risk of coronary events in subjects with elevated levels of CRP.
AbstractList	Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exert direct pro-atherosclerotic effects. Therefore, we aimed at determining whether CRP might induce MMP-9 in two different experimental conditions: 1) smooth muscle cells (SMCs) in vitro, and 2) patients with ACS. Effects of increasing concentrations of CRP on MMP-9 expression were evaluated in vitro in human SMCs. TIMP-1 protein expression, the selective inhibitor of MMP-9, was also evaluated. CRP dose-dependently induced MMP-9 expression in SMCs by promoting MMP-mRNA transcription, as well as MMP-9 secretion. In contrast, no differences were found for TIMP-1 protein expression. In vivo, MMP-9 and CRP levels were measured in blood samples obtained from the aorta (Ao) and the coronary sinus (Cs) of patients with normal coronary arteries (controls, n=21), stable angina (n=24), and ACS (n=30). Both MMP-9 and CRP plasma levels were significantly increased across the coronary circulation only in patients with ACS. Interestingly, a significant correlation between MMP-9 and CRP plasma levels was found. CRP induced MMP-9 expression and activity in human SMCs in culture; patients presenting with ACS have increased transcoronary plasma levels of MMP-9 and CRP with a significant correlation between these two markers. This may explain the heightened risk of coronary events in subjects with elevated levels of CRP. Abstract Background Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exert direct pro-atherosclerotic effects. Therefore, we aimed at determining whether CRP might induce MMP-9 in two different experimental conditions: 1) smooth muscle cells (SMCs) in vitro, and 2) patients with ACS. Methods and results Effects of increasing concentrations of CRP on MMP-9 expression were evaluated in vitro in human SMCs. TIMP-1 protein expression, the selective inhibitor of MMP-9, was also evaluated. CRP dose-dependently induced MMP-9 expression in SMCs by promoting MMP-mRNA transcription, as well as MMP-9 secretion. In contrast, no differences were found for TIMP-1 protein expression. In vivo, MMP-9 and CRP levels were measured in blood samples obtained from the aorta (Ao) and the coronary sinus (Cs) of patients with normal coronary arteries (controls, n = 21), stable angina (n = 24), and ACS (n = 30). Both MMP-9 and CRP plasma levels were significantly increased across the coronary circulation only in patients with ACS. Interestingly, a significant correlation between MMP-9 and CRP plasma levels was found. Conclusions CRP induced MMP-9 expression and activity in human SMCs in culture; patients presenting with ACS have increased transcoronary plasma levels of MMP-9 and CRP with a significant correlation between these two markers. This may explain the heightened risk of coronary events in subjects with elevated levels of CRP. Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exert direct pro-atherosclerotic effects. Therefore, we aimed at determining whether CRP might induce MMP-9 in two different experimental conditions: 1) smooth muscle cells (SMCs) in vitro, and 2) patients with ACS.BACKGROUNDMatrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms responsible for MMP expression in ACS. C-reactive protein (CRP) not only is an independent risk factor for cardiovascular events, but also may exert direct pro-atherosclerotic effects. Therefore, we aimed at determining whether CRP might induce MMP-9 in two different experimental conditions: 1) smooth muscle cells (SMCs) in vitro, and 2) patients with ACS.Effects of increasing concentrations of CRP on MMP-9 expression were evaluated in vitro in human SMCs. TIMP-1 protein expression, the selective inhibitor of MMP-9, was also evaluated. CRP dose-dependently induced MMP-9 expression in SMCs by promoting MMP-mRNA transcription, as well as MMP-9 secretion. In contrast, no differences were found for TIMP-1 protein expression. In vivo, MMP-9 and CRP levels were measured in blood samples obtained from the aorta (Ao) and the coronary sinus (Cs) of patients with normal coronary arteries (controls, n=21), stable angina (n=24), and ACS (n=30). Both MMP-9 and CRP plasma levels were significantly increased across the coronary circulation only in patients with ACS. Interestingly, a significant correlation between MMP-9 and CRP plasma levels was found.METHODS AND RESULTSEffects of increasing concentrations of CRP on MMP-9 expression were evaluated in vitro in human SMCs. TIMP-1 protein expression, the selective inhibitor of MMP-9, was also evaluated. CRP dose-dependently induced MMP-9 expression in SMCs by promoting MMP-mRNA transcription, as well as MMP-9 secretion. In contrast, no differences were found for TIMP-1 protein expression. In vivo, MMP-9 and CRP levels were measured in blood samples obtained from the aorta (Ao) and the coronary sinus (Cs) of patients with normal coronary arteries (controls, n=21), stable angina (n=24), and ACS (n=30). Both MMP-9 and CRP plasma levels were significantly increased across the coronary circulation only in patients with ACS. Interestingly, a significant correlation between MMP-9 and CRP plasma levels was found.CRP induced MMP-9 expression and activity in human SMCs in culture; patients presenting with ACS have increased transcoronary plasma levels of MMP-9 and CRP with a significant correlation between these two markers. This may explain the heightened risk of coronary events in subjects with elevated levels of CRP.CONCLUSIONSCRP induced MMP-9 expression and activity in human SMCs in culture; patients presenting with ACS have increased transcoronary plasma levels of MMP-9 and CRP with a significant correlation between these two markers. This may explain the heightened risk of coronary events in subjects with elevated levels of CRP.
Author	Cirillo, Plinio Golino, Paolo Loffredo, Francesco Ragni, Massimo Gresele, Paolo Falcinelli, Emanuela Petrillo, Gianluca Chiariello, Massimo Cimmino, Giovanni
Author_xml	– sequence: 1 givenname: Giovanni surname: Cimmino fullname: Cimmino, Giovanni organization: Department of Cardiothoracic and Respiratory Sciences, Division of Cardiology, Second University of Naples, Naples, Italy – sequence: 2 givenname: Massimo surname: Ragni fullname: Ragni, Massimo organization: Division of Cardiology, Umberto I Hospital, Nocera Inferiore, Italy – sequence: 3 givenname: Plinio surname: Cirillo fullname: Cirillo, Plinio organization: Department of Internal Medicine, Cardiovascular and Immunological Sciences, Division of Cardiology, University of Naples “Federico II”, Naples, Italy – sequence: 4 givenname: Gianluca surname: Petrillo fullname: Petrillo, Gianluca organization: Department of Internal Medicine, Cardiovascular and Immunological Sciences, Division of Cardiology, University of Naples “Federico II”, Naples, Italy – sequence: 5 givenname: Francesco surname: Loffredo fullname: Loffredo, Francesco organization: Department of Cardiothoracic and Respiratory Sciences, Division of Cardiology, Second University of Naples, Naples, Italy – sequence: 6 givenname: Massimo surname: Chiariello fullname: Chiariello, Massimo organization: Department of Internal Medicine, Cardiovascular and Immunological Sciences, Division of Cardiology, University of Naples “Federico II”, Naples, Italy – sequence: 7 givenname: Paolo surname: Gresele fullname: Gresele, Paolo organization: Department of Internal and Vascular Medicine, Division of Internal Medicine, University of Perugia, Italy – sequence: 8 givenname: Emanuela surname: Falcinelli fullname: Falcinelli, Emanuela organization: Department of Internal and Vascular Medicine, Division of Internal Medicine, University of Perugia, Italy – sequence: 9 givenname: Paolo surname: Golino fullname: Golino, Paolo email: paolo.golino@unina2.it organization: Department of Cardiothoracic and Respiratory Sciences, Division of Cardiology, Second University of Naples, Naples, Italy
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Keywords	CRP Acute coronary syndromes MMP-9 Enzyme Rupture Metalloendopeptidases Cardiovascular disease Inflammation Gene expression Coronary heart disease Myocardial disease Gelatinase B Peptidases Acute phase protein Hydrolases Cardiology C reactive protein Acute coronary syndrome
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Snippet	Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about the mechanisms... Abstract Background Matrix metalloproteases (MMPs) have been implicated in the pathogenesis of acute coronary syndromes (ACS). However, little is known about...
SourceID	proquest pubmed pascalfrancis crossref elsevier
SourceType	Aggregation Database Index Database Enrichment Source Publisher
StartPage	981
SubjectTerms	Acute Coronary Syndrome - enzymology Acute Coronary Syndrome - genetics Acute Coronary Syndrome - metabolism Acute coronary syndromes Aged Biological and medical sciences C-Reactive Protein - metabolism C-Reactive Protein - physiology Cardiology. Vascular system Cardiovascular Cells, Cultured Coronary heart disease CRP Female Gene Expression Regulation, Enzymologic Heart Humans Inflammation - enzymology Inflammation - genetics Inflammation - metabolism Male Matrix Metalloproteinase 9 - biosynthesis Matrix Metalloproteinase 9 - genetics Medical sciences Middle Aged MMP-9 Muscle, Smooth, Vascular - enzymology Muscle, Smooth, Vascular - metabolism Myocarditis. Cardiomyopathies Myocytes, Smooth Muscle - enzymology Myocytes, Smooth Muscle - pathology Plaque, Atherosclerotic - blood Plaque, Atherosclerotic - enzymology Plaque, Atherosclerotic - metabolism Up-Regulation - genetics
Title	C-reactive protein induces expression of matrix metalloproteinase-9: A possible link between inflammation and plaque rupture
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Volume	168
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