10 results on '"IALENTI, ARMANDO"'
Search Results
2. Plasmacytoid Dendritic Cells Play a Key Role in Promoting Atherosclerosis in Apolipoprotein E-Deficient Mice.
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MacRitchie, Neil, Grassia, Gianluca, Sabir, Suleman R., Maddaluno, Marcella, Welsh, Paul, Sattar, Naveed, Ialenti, Armando, Kurowska-Stolarska, Mariola, McInnes, Iain B., Brewer, James M., Garside, Paul, and Maffia, Pasquale
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- 2012
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3. The IκB Kinase Inhibitor Nuclear Factor-κB Essential Modulator-Binding Domain Peptide for Inhibition of Injury-Induced Neointimal Formation.
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Grassia, Gianluca, Maddaluno, Marcella, Musilli, Claudia, De Stefano, Daniela, Carnuccio, Rosa, Vittoria Di Lauro, Maria, Parratt, Christopher A., Kennedy, Simon, Di Meglio, Paola, Ianaro, Angela, Maffia, Pasquale, Parenti, Astrid, and Ialenti, Armando
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- 2010
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4. Reply.
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Iuvone, Teresa, Affaitati, Giannapia, Filippis, Daniele De, Lopopolo, Mariangela, Grassi, Gianluca, Lapenna, Domenico, Negro, Luana, Costantini, Raffaele, Vaia, Massimo, Cipollone, Francesco, Ialenti, Armando, Giamberardin, Maria Adele, De Filippis, Daniele, and Giamberardino, Maria Adele
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- 2016
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5. Matrix metalloproteinase-8 promotes vascular smooth muscle cell proliferation and neointima formation.
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Xiao Q, Zhang F, Grassia G, Hu Y, Zhang Z, Xing Q, Yin X, Maddaluno M, Drung B, Schmidt B, Maffia P, Ialenti A, Mayr M, Xu Q, and Ye S
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- ADAM Proteins antagonists & inhibitors, ADAM Proteins genetics, ADAM Proteins metabolism, ADAM10 Protein, Amyloid Precursor Protein Secretases antagonists & inhibitors, Amyloid Precursor Protein Secretases genetics, Amyloid Precursor Protein Secretases metabolism, Animals, Apolipoproteins E deficiency, Apolipoproteins E genetics, Cadherins metabolism, Carotid Artery Injuries genetics, Cell Movement, Cells, Cultured, Culture Media, Conditioned metabolism, Cyclin D1 metabolism, Disease Models, Animal, Matrix Metalloproteinase 8 deficiency, Matrix Metalloproteinase 8 genetics, Matrix Metalloproteinase Inhibitors pharmacology, Membrane Proteins antagonists & inhibitors, Membrane Proteins genetics, Membrane Proteins metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Muscle, Smooth, Vascular drug effects, Muscle, Smooth, Vascular pathology, Myocytes, Smooth Muscle drug effects, Myocytes, Smooth Muscle pathology, Proteomics methods, RNA Interference, Time Factors, Transfection, Wnt Signaling Pathway, Wnt1 Protein metabolism, beta Catenin metabolism, Carotid Artery Injuries enzymology, Carotid Artery Injuries pathology, Cell Proliferation drug effects, Matrix Metalloproteinase 8 metabolism, Muscle, Smooth, Vascular enzymology, Myocytes, Smooth Muscle enzymology, Neointima
- Abstract
Objective: We investigated the role of matrix metalloproteinase-8 (MMP8) in neointima formation and in vascular smooth muscle cell (VSMC) migration and proliferation., Approach and Results: After carotid artery wire injuring, MMP8(-/-)/apoE(-/-) mice had fewer proliferating cells in neointimal lesions and smaller lesion sizes. Ex vivo assays comparing VSMCs isolated from MMP8 knockout and wild-type mice showed that MMP8 knockout decreased proliferation and migration. Proteomics analysis revealed that a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) had lower concentrations in MMP8 knockout VSMC culture media than in MMP8 wild-type VSMC culture media. Western blot, flow cytometric, and immunocytochemical analyses showed that MMP8 knockout VSMCs contained more pro-ADAM10 but less mature ADAM10, more N-cadherin, and β-catenin in the plasma membrane but less β-catenin in the nucleus and less cyclin D1. Treatment of MMP8 wild-type VSMCs with an ADAM10 inhibitor, GI254023X, or siRNA knockdown of ADAM10 in MMP8 wild-type VSMCs inhibited proliferation and migration, increased N-cadherin and β-catenin in the plasma membrane, reduced β-catenin in the nucleus, and decreased cyclin D1 expression. Incubation of MMP8 knockout VSMCs with a recombinant ADAM10 rescued the proliferative and migratory ability of MMP8 knockout VSMCs and increased cyclin D1 expression. Furthermore, immunohistochemical analyses showed colocalization of ADAM10 with VSMCs and N-cadherin, and nuclear accumulation of β-catenin in the neointima in apoE(-/-)/MMP8(+/+) mice., Conclusions: MMP8 enhances VSMC proliferation via an ADAM10, N-cadherin, and β-catenin-mediated pathway and plays an important role in neointima formation.
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- 2014
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6. Inhibition of in-stent stenosis by oral administration of bindarit in porcine coronary arteries.
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Ialenti A, Grassia G, Gordon P, Maddaluno M, Di Lauro MV, Baker AH, Guglielmotti A, Colombo A, Biondi G, Kennedy S, and Maffia P
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- Administration, Oral, Animals, Cell Proliferation drug effects, Coronary Stenosis pathology, Coronary Vessels drug effects, Indazoles pharmacology, Male, Models, Animal, Monocyte Chemoattractant Proteins antagonists & inhibitors, Monocyte Chemoattractant Proteins blood, Muscle, Smooth, Vascular drug effects, Muscle, Smooth, Vascular pathology, Neointima pathology, Neointima prevention & control, Propionates pharmacology, Swine, Treatment Outcome, Coronary Stenosis prevention & control, Coronary Vessels pathology, Indazoles administration & dosage, Indazoles therapeutic use, Propionates administration & dosage, Propionates therapeutic use, Stents
- Abstract
Objective: We have previously demonstrated that bindarit, a selective inhibitor of monocyte chemotactic proteins (MCPs), is effective in reducing neointimal formation in rodent models of vascular injury by reducing smooth muscle cell proliferation and migration and neointimal macrophage content, effects associated with the inhibition of MCP-1/CCL2 production. The aim of the current study was to evaluate the efficacy of bindarit on in-stent stenosis in the preclinical porcine coronary stent model., Methods and Results: One or 2 bare metal stents (Multi-Link Vision, 3.5 mm) were deployed (1:1.2 oversize ratio) in the coronary arteries of 42 pigs (20 bindarit versus 22 controls). Bindarit (50 mg/kg per day) was administered orally from 2 days before stenting until the time of euthanasia at 7 and 28 days. Bindarit caused a significant reduction in neointimal area (39.4%, P<0.001, n=9 group), neointimal thickness (51%, P<0.001), stenosis area (37%, P<0.001), and inflammatory score (40%, P<0.001) compared with control animals, whereas there was no significant difference in the injury score between the 2 groups. Moreover, treatment with bindarit significantly reduced the number of proliferating cells (by 45%, P<0.05; n=6 group) and monocyte/macrophage content (by 55%, P<0.01; n=5-6 group) in stented arteries at day 7 and 28, respectively. These effects were associated with a significant (P<0.05) reduction of MCP-1 plasma levels at day 28. In vitro data showed that bindarit (10-300 μmol/L) reduced tumor necrosis factor-α (50 ng/mL)-induced pig coronary artery smooth muscle cell proliferation and inhibited MCP-1 production., Conclusion: Our results show the efficacy of bindarit in the prevention of porcine in-stent stenosis and support further investigation for clinical application of this compound.
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- 2011
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7. The I{kappa}B kinase inhibitor nuclear factor-{kappa}B essential modulator-binding domain peptide for inhibition of injury-induced neointimal formation.
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Grassia G, Maddaluno M, Musilli C, De Stefano D, Carnuccio R, Di Lauro MV, Parratt CA, Kennedy S, Di Meglio P, Ianaro A, Maffia P, Parenti A, and Ialenti A
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- Angioplasty, Balloon adverse effects, Animals, Apolipoproteins E deficiency, Apolipoproteins E genetics, Apoptosis drug effects, Carotid Artery Injuries enzymology, Carotid Artery Injuries etiology, Carotid Artery Injuries pathology, Cell Movement drug effects, Cell Proliferation drug effects, Cells, Cultured, Chemokine CCL2 metabolism, Disease Models, Animal, Dose-Response Relationship, Drug, Enzyme Activation, Female, Hyperplasia, I-kappa B Kinase metabolism, Male, Matrix Metalloproteinase 2 metabolism, Matrix Metalloproteinase 9 metabolism, Mice, Mice, Knockout, Myocytes, Smooth Muscle enzymology, Myocytes, Smooth Muscle pathology, NF-kappa B metabolism, Phosphorylation, Rats, Rats, Wistar, Tunica Intima enzymology, Tunica Intima pathology, Carotid Artery Injuries prevention & control, I-kappa B Kinase antagonists & inhibitors, Intracellular Signaling Peptides and Proteins metabolism, Myocytes, Smooth Muscle drug effects, Peptides pharmacology, Protein Kinase Inhibitors pharmacology, Tunica Intima drug effects
- Abstract
Objective: The activation of nuclear factor-κB (NF-κB) is a crucial step in the arterial wall's response to injury. The identification and characterization of the NF-κB essential modulator-binding domain (NBD) peptide, which can block the activation of the IκB kinase complex, have provided an opportunity to selectively abrogate the inflammation-induced activation of NF-κB. The aim of the present study was to evaluate the effect of the NBD peptide on neointimal formation., Methods and Results: In the rat carotid artery balloon angioplasty model, local treatment with the NBD peptide (300 μg/site) significantly reduced the number of proliferating cells at day 7 (by 40%; P<0.01) and reduced injury-induced neointimal formation (by 50%; P<0.01) at day 14. These effects were associated with a significant reduction of NF-κB activation and monocyte chemotactic protein-1 expression in the carotid arteries of rats treated with the peptide. In addition, the NBD peptide (0.01 to 1 μmol/L) reduced rat smooth muscle cell proliferation, migration, and invasion in vitro. Similar results were observed in apolipoprotein E(-/-) mice in which the NBD peptide (150 μg/site) reduced wire-induced neointimal formation at day 28 (by 47%; P<0.01)., Conclusions: The NBD peptide reduces neointimal formation and smooth muscle cell proliferation/migration, both effects associated with the inhibition of NF-κB activation.
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- 2010
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8. Images in cardiovascular medicine. Multiphoton microscopy for 3-dimensional imaging of lymphocyte recruitment into apolipoprotein-E-deficient mouse carotid artery.
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Maffia P, Zinselmeyer BH, Ialenti A, Kennedy S, Baker AH, McInnes IB, Brewer JM, and Garside P
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- Animals, Apolipoproteins E deficiency, Cells, Cultured, Chemotaxis, Leukocyte immunology, Female, Lymph Nodes cytology, Lymphocytes pathology, Mice, Mice, Inbred C57BL, Mice, Mutant Strains, Vasculitis immunology, Vasculitis pathology, Apolipoproteins E genetics, Carotid Artery Diseases immunology, Carotid Artery Diseases pathology, Imaging, Three-Dimensional, Microscopy, Fluorescence, Multiphoton
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- 2007
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9. Neutralization of interleukin-18 inhibits neointimal formation in a rat model of vascular injury.
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Maffia P, Grassia G, Di Meglio P, Carnuccio R, Berrino L, Garside P, Ianaro A, and Ialenti A
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- Actins analysis, Animals, Balloon Occlusion adverse effects, Carotid Arteries chemistry, Carotid Arteries pathology, Carotid Arteries physiopathology, Carotid Artery Injuries pathology, Cell Movement drug effects, Cell Movement physiology, Cell Proliferation drug effects, Disease Models, Animal, Endothelium, Vascular injuries, Endothelium, Vascular pathology, Endothelium, Vascular physiopathology, Gene Expression Regulation drug effects, Gene Expression Regulation physiology, Immunoglobulin G pharmacology, Interferon-gamma analysis, Interferon-gamma genetics, Interferon-gamma physiology, Interleukin-18 analysis, Interleukin-18 blood, Interleukin-18 genetics, Interleukin-6 analysis, Interleukin-6 genetics, Interleukin-6 physiology, Interleukin-8 analysis, Interleukin-8 genetics, Interleukin-8 physiology, Male, Muscle, Smooth, Vascular pathology, Muscle, Smooth, Vascular physiopathology, NF-kappa B analysis, NF-kappa B physiology, RNA, Messenger analysis, RNA, Messenger genetics, Rats, Rats, Wistar, Time Factors, Tunica Intima pathology, Cardiovascular Diseases physiopathology, Carotid Artery Injuries etiology, Carotid Artery Injuries physiopathology, Interleukin-18 physiology, Tunica Intima physiopathology
- Abstract
Background: Studies in humans and animal models suggest that interleukin-18 (IL-18) plays a crucial role in vascular pathologies. IL-18 is a predictor of cardiovascular death in angina and is involved in atherotic plaque destabilization. Higher IL-18 plasma levels also are associated with restenosis after coronary artery angioplasty performed in patients with acute myocardial infarction. We investigated the effective role of IL-18 in neointimal formation in a balloon-induced rat model of vascular injury., Methods and Results: Endothelial denudation of the left carotid artery was performed by use of a balloon embolectomy catheter. Increased expression of IL-18 and IL-18Ralpha/beta mRNA was detectable in carotid arteries from days 2 to 14 after angioplasty. The active form of IL-18 was highly expressed in injured arteries. Strong immunoreactivity for IL-18 was detected in the medial smooth muscle cells at days 2 and 7 after balloon injury and in proliferating/migrating smooth muscle cells in neointima at day 14. Moreover, serum concentrations of IL-18 were significantly higher among rats subjected to vascular injury. Treatment with neutralizing rabbit anti-rat IL-18 immunoglobulin G significantly reduced neointimal formation (by 27%; P < 0.01), reduced the number of proliferating cells, and inhibited interferon-gamma, IL-6, and IL-8 mRNA expression and nuclear factor-kappaB activation in injured arteries. In addition, in vitro data show that IL-18 affects smooth muscle cell proliferation., Conclusions: These results identify a critical role for IL-18 in neointimal formation in a rat model of vascular injury and suggest a potential role for IL-18 neutralization in the reduction of neointimal development.
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- 2006
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10. Beneficial effects of NO-releasing derivative of flurbiprofen (HCT-1026) in rat model of vascular injury and restenosis.
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Maffia P, Ianaro A, Sorrentino R, Lippolis L, Maiello FM, del Soldato P, Ialenti A, and Cirino G
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- Administration, Oral, Angioplasty, Balloon, Coronary adverse effects, Animals, Carotid Arteries enzymology, Carotid Arteries pathology, Coronary Restenosis etiology, Dose-Response Relationship, Drug, Hyperplasia prevention & control, Immunohistochemistry, Male, Nitric Oxide Synthase drug effects, Nitric Oxide Synthase Type II, Proliferating Cell Nuclear Antigen analysis, Rats, Rats, Wistar, Stomach Diseases chemically induced, Stomach Diseases pathology, Tunica Intima pathology, Tunica Intima physiopathology, Anti-Inflammatory Agents, Non-Steroidal pharmacology, Coronary Restenosis prevention & control, Flurbiprofen analogs & derivatives, Flurbiprofen pharmacology, Nitric Oxide blood, Tunica Intima drug effects
- Abstract
One of the major problems related to the percutaneous transluminal coronary angioplasty technique is the renarrowing of the vessel, a phenomenon known as restenosis. NO and nonsteroidal anti-inflammatory drugs have been shown to play a role in this pathology. The main problem with the use of conventional NO donors is that they affect blood pressure and flow, and for these reasons, they cannot be used safely in clinical practice. The aim of this study was to evaluate, with the use of a rat model of balloon angioplasty, whether a structural derivative of flurbiprofen, containing an added NO-releasing moiety (HCT-1026), is able to reduce or prevent neointimal formation. Rats were treated for 14 days with equimolar doses of flurbiprofen (2, 7, and 21 mg/kg) or HCT-1026 (3, 10, and 30 mg/kg). After this 14-day treatment, HCT-1026 but not flurbiprofen significantly modified the neointima/media ratio. The reduction in the neointimal proliferation obtained with HCT-1026 was well correlated with an increase in nitrite/nitrate plasma levels and a reduced cell proliferation. Neither HCT-1026 nor flurbiprofen affected inducible NO synthase induction in injured vessels. In conclusion, HCT-1026 caused a significant reduction in restenosis that appears to be directly related to NO release. HCT-1026 may prove to be beneficial in preventing or delaying restenosis in humans.
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- 2002
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