Matrix Metalloproteinases and Vulnerable Atheromatous Plaque

Toutouzas, Konstantinos; Synetos, Αndreas; Nikolaou, Charalampia; Tsiamis, Eleutherios; Tousoulis, Dimitris; Stefanadis, Christodoulos

doi:10.2174/1568026611208011166

Cited by 25 publications

(10 citation statements)

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“…The aortic expression of MMP-2 and MMP-9 was increased in the later stages of atherosclerosis progression. As reported previously, MMP-2 and MMP-9 are mainly expressed in advanced atherosclerotic plaque in a mouse model (28) , and have been shown to induce carotid plaque instability (29) .…”

Section: Cd68 Cd36supporting

confidence: 70%

Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation

et al. 2014

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In the present study, the anti-atherosclerotic effect and the underlying mechanism of curcuma oil (C. oil), a lipophilic fraction from turmeric (Curcuma longa L.), was evaluated in a hamster model of accelerated atherosclerosis and in THP-1 macrophages. Male golden Syrian hamsters were subjected to partial carotid ligation (PCL) or FeCl 3 -induced arterial oxidative injury (Ox-injury) after 1 week of treatment with a high-cholesterol (HC) diet or HC diet plus C. oil (100 and 300 mg/kg, orally). Hamsters fed with the HC diet were analysed at 1, 3 and 5 weeks following carotid injury. The HC diet plus C. oil-fed group was analysed at 5 weeks. In hyperlipidaemic hamsters with PCL or Ox-injury, C. oil (300 mg/kg) reduced elevated plasma and aortic lipid levels, arterial macrophage accumulation, and stenosis when compared with those subjected to arterial injury alone. Similarly, elevated mRNA transcripts of matrix metalloproteinase-2 (MMP-2), MMP-9, cluster of differentiation 45 (CD45), TNF-a, interferon-g (IFN-g), IL-1b and IL-6 were reduced in atherosclerotic arteries, while those of transforming growth factor-b (TGF-b) and IL-10 were increased after the C. oil treatment (300 mg/kg). The treatment with C. oil prevented HC diet-and oxidised LDL (OxLDL)-induced lipid accumulation, decreased the mRNA expression of CD68 and CD36, and increased the mRNA expression of PPARa, LXRa, ABCA1 and ABCG1 in both hyperlipidaemic hamster-derived peritoneal and THP-1 macrophages. The administration of C. oil suppressed the mRNA expression of TNF-a, IL-1b, IL-6 and IFN-g and increased the expression of TGF-b in peritoneal macrophages. In THP-1 macrophages, C. oil supplementation prevented OxLDL-induced production of TNF-a and IL-1b and increased the levels of TGF-b. The present study shows that C. oil attenuates arterial injury-induced accelerated atherosclerosis, inflammation and macrophage foam-cell formation.

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Section: Cd68 Cd36supporting

confidence: 70%

Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation

et al. 2014

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“…Monocytes contribute directly to atherosclerosis as effectors of innate immunity. MMPs are involved in the monocyte functions [44] and participate in the destabilization of atherosclerotic plaques [45,46]. Moreover, MMPs can degrade extracellular matrix (ECM) proteins and are implicated in the dysfunction of connective tissue and remodelling of atherosclerotic lesions [47,48].…”

Section: Discussionmentioning

confidence: 99%

The serum protein fetuin-B is involved in the development of acute myocardial infarction

et al. 2015

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The rupture of an atherosclerotic plaque is one of the main causes of coronary artery thrombotic occlusion, leading to myocardial infarction. However, the exact mechanism and causal risk factors for plaque rupture remain unclear. To identify a potential molecule that can influence atherosclerotic plaque rupture, we investigated protein expression in serum from patients with acute myocardial infarction (AMI) and stable angina (SA), using proteomic analysis. The expression of six proteins, including fibrinogen, fetuin-B, keratin 9, proapolipoprotein and fibrinogen, were altered in serum from patients with AMI compared with serum from those with SA. Of these, fetuin-B, proapolipoprotein, fibrinogen γ-B-chain precursors and fibrinogen expression were greater in serum from patients with AMI than from patients with SA. Increased fetuin-B expression in serum from AMI patients was also confirmed by Western blot analysis. Treatment with recombinant human fetuin-B increased the migration in monocytes and macrophages in a concentration-dependent manner. Fetuin-B also affected vascular plaque-stabilizing factors, including lipid deposition and cytokine production in macrophages, the activation of matrix metalloproteinase (MMP)-2 in monocytes, and the activation of apoptosis and MMP-2 in vascular smooth muscle cells. Moreover, in vivo administration of fetuin-B decreased the collagen accumulation and smooth muscle cell content and showed an increased number of macrophages in the vascular plaque. From these results, we suggest that fetuin-B may act as a modulator in the development of AMI. This study may provide a therapeutic advantage for patients at high risk of AMI.

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“…Extrinsic features include increased blood pressure, hemodynamic shear stress, and vasospam [62,[70][71][72][73][74]. Plaque rupture tends to occur at the shoulder region, which is associated with cap thinning and macrophage infiltration [75]; the shoulder region is also the area of the plaque exposed to the greatest shear stress [74]. Macrophages control many of the inflammatory processes within the plaque, and are the principal cells responsible for the production of MMPs [49].…”

Section: Introductionmentioning

confidence: 99%

Metalloproteinases and Metalloproteinase Inhibitors in Age-Related Diseases

Gargiulo¹,

Gamba²,

Poli³

et al. 2014

CPD

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Degradation of the extracellular matrix is an important feature of embryonic development, morphogenesis, angiogenesis, tissue repair and remodeling. It is precisely regulated under physiological conditions, but when dysregulated it becomes a cause of many diseases, including atherosclerosis, osteoarthritis, diabetic vascular complications, and neurodegeneration. Various types of proteinases are implicated in extracellular matrix degradation, but the major enzymes are considered to be metalloproteinases such as matrix metalloproteinases (MMPs) and disintegrin and metalloproteinase domain (ADAMs) that include ADAMs with a thrombospondin domain (ADAMTS).This review discusses involvement of the major metalloproteinases in some age-related chronic diseases, and examines what is currently known about the beneficial effects of their inhibitors, used as new therapeutic strategies for treating or preventing the development and progression of these diseases.

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Matrix Metalloproteinases and Vulnerable Atheromatous Plaque

Cited by 25 publications

References 0 publications

Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation

Curcuma oil attenuates accelerated atherosclerosis and macrophage foam-cell formation by modulating genes involved in plaque stability, lipid homeostasis and inflammation

The serum protein fetuin-B is involved in the development of acute myocardial infarction

Metalloproteinases and Metalloproteinase Inhibitors in Age-Related Diseases

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