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Search Results: 1 - 10 of 2148 matches for " Badimon Lina "
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Atherosclerosis and Thrombosis: Insights from Large Animal Models
Gemma Vilahur,Teresa Padro,Lina Badimon
Journal of Biomedicine and Biotechnology , 2011, DOI: 10.1155/2011/907575
Abstract: Atherosclerosis and its thrombotic complications are responsible for remarkably high numbers of deaths. The combination of in vitro, ex vivo, and in vivo experimental approaches has largely contributed to a better understanding of the mechanisms underlying the atherothrombotic process. Indeed, different animal models have been implemented in atherosclerosis and thrombosis research in order to provide new insights into the mechanisms that have already been outlined in isolated cells and protein studies. Yet, although no model completely mimics the human pathology, large animal models have demonstrated better suitability for translation to humans. Indeed, direct translation from mice to humans should be taken with caution because of the well-reported species-related differences. This paper provides an overview of the available atherothrombotic-like animal models, with a particular focus on large animal models of thrombosis and atherosclerosis, and examines their applicability for translational research purposes as well as highlights species-related differences with humans.
Controlling the angiogenic switch in developing atherosclerotic plaques: Possible targets for therapeutic intervention
Mark Slevin, Jerzy Krupinski, Lina Badimon
Vascular Cell , 2009, DOI: 10.1186/2040-2384-1-4
Abstract: In recent years, an increasing number of angiogenic therapeutic targets have been proposed in order to facilitate modulation of neovascularization and its consequences in diseases such as cancer and macular degeneration. A complete knowledge of the mechanisms responsible for initiation of adventitial vessel proliferation, their extension into the intimal regions and possible de-novo synthesis of neovessels following differentiation of bone-marrow-derived stem cells is required in order to contemplate potential single or combinational anti-angiogenic therapies. In this review, we will examine the importance of angiogenesis in complicated plaque development, describe the current knowledge of molecular mechanisms of its initiation and maintenance, and discuss possible future anti-angiogenic therapies to control plaque stability.According to a World Health Organization Fact Sheet (EURO/03/06) cardiovascular disease (CVD) is the number one killer in Europe, with heart disease and stroke being the major cause of death in all 53 Member States. Figures show that 34,421 (23% of all non-communicable diseases) of Europeans died from CVD in 2005. The report also highlighted the fact that there is approximately a 10-fold difference in premature CVD mortality between Western Europe and countries in Central and Eastern Europe with a higher occurrence of CVD amongst the poor and vulnerable. Although improvements in understanding have helped to reduce the number of Western European dying from CVD and related diseases further advances will require a clearer understanding of the pathobiological mechanisms responsible for the development of stroke, atherosclerosis and myocardial infarction. Approximately 75% of acute coronary events and 60% of symptomatic carotid artery disease are associated with disruption of atherosclerotic plaques [1]. In 1971, Folkman [2]introduced the concept of angiogenesis as a necessity for tumour growth. Its importance in other pathological conditions, includ
Unique vascular protective properties of natural products: supplements or future main-line drugs with significant anti-atherosclerotic potential?
mark slevin, Nessar Ahmed, Quiyu Wang, Garry Mcdowell, Lina Badimon
Vascular Cell , 2012, DOI: 10.1186/2045-824x-4-9
CD105 positive neovessels are prevalent in early stage carotid lesions, and correlate with the grade in more advanced carotid and coronary plaques
Ana Luque, Mark Slevin, Marta M Turu, Oriol Juan-Babot, Lina Badimon, Jerzy Krupinski
Vascular Cell , 2009, DOI: 10.1186/2040-2384-1-6
Abstract: We have used immunohistochemical analysis to investigate the expression of CD105-positive vessels in both large (carotid) and medium calibre (coronary and middle cerebral artery, MCAs) diseased vessels in an attempt to identify any correlation with plaque growth, stage and complication/type.Here we show, that carotid arteries expressed intimal neovascularization associated with CD105-positive endothelial cells, concomitant with increased inflammation in early stage lesions, preatheroma (I-III) whilst they were not present in coronary plaques of the same grade. Some of these CD105-positive neovessels were immature, thin walled and without smooth muscle cell coverage making them more prone to haemorrhage and rupture. In high-grade lesions, neovessel proliferation was similar in both arterial types and significantly higher numbers of CD105-positive vasa vasorum were associated with plaque regions in coronary arteries. In contrast, although the MCAs exhibited expanded intimas and established plaques, there were very few CD105 positive neovessels.Our results show that CD105 is a useful marker of angiogenesis within adventitial and intimal vessels and suggest the existence of significant differences in the pathological development of atherosclerosis in separate vascular beds which may have important consequences when considering management and treatment of this disease.Atherosclerosis is strongly associated with symptomatic cardiovascular disease and ischemic stroke, which are the leading causes of death and disability in the Western world. Atherosclerosis is considered to be a multifactorial disease with numerous risk factors including smoking, alcohol abuse, hypertension, diabetes mellitus, dyslipidemia and infection with microorganisms including Chlamydia pneumoniae [1]. All these factors involve complex interactions between pathways associated with inflammation, lipid metabolism, coagulation, hypoxia, apoptosis and the immune response. Atherosclerotic plaque instabili
LDL-Induced Impairment of Human Vascular Smooth Muscle Cells Repair Function Is Reversed by HMG-CoA Reductase Inhibition
Teresa Padró, Roberta Lugano, Maisa García-Arguinzonis, Lina Badimon
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038935
Abstract: Growing human atherosclerotic plaques show a progressive loss of vascular smooth muscle cells (VSMC) becoming soft and vulnerable. Lipid loaded-VSMC show impaired vascular repair function and motility due to changes in cytoskeleton proteins involved in cell-migration. Clinical benefits of statins reducing coronary events have been related to repopulation of vulnerable plaques with VSMC. Here, we investigated whether HMG-CoA reductase inhibition with rosuvastatin can reverse the effects induced by atherogenic concentrations of LDL either in the native (nLDL) form or modified by aggregation (agLDL) on human VSMC motility. Using a model of wound repair, we showed that treatment of human coronary VSMC with rosuvastatin significantly prevented (and reversed) the inhibitory effect of nLDL and agLDL in the repair of the cell depleted areas. In addition, rosuvastatin significantly abolished the agLDL-induced dephosphorylation of myosin regulatory light chain as demonstrated by 2DE-electrophoresis and mass spectrometry. Besides, confocal microscopy showed that rosuvastatin enhances actin-cytoskeleton reorganization during lipid-loaded-VSMC attachment and spreading. The effects of rosuvastatin on actin-cytoskeleton dynamics and cell migration were dependent on ROCK-signalling. Furthermore, rosuvastatin caused a significant increase in RhoA-GTP in the cytosol of VSMC. Taken together, our study demonstrated that inhibition of HMG-CoA reductase restores the migratory capacity and repair function of VSMC that is impaired by native and aggregated LDL. This mechanism may contribute to the stabilization of lipid-rich atherosclerotic plaques afforded by statins.
Conformation and Physical Structure of Tropoelastin from Human Vascular Cells: Influence of Cells Lipid Loading
Valerie Samouillan,Jany Dandurand,Laura Nasarre,Lina Badimon,Colette Lacabanne,Vicenta Llorente-Cortés
Conference Papers in Science , 2014, DOI: 10.1155/2014/391242
Abstract: Aggregated low density lipoproteins (agLDL) contribute to massive intracellular cholesteryl ester (CE) accumulation in human vascular smooth muscle cells (VSMC). Our aim was to determine the conformational and physical structure of agLDL and elastic material produced either by control human VSMC or by agLDL-loaded human VSMC (agLDL-VSMC). At the conformational level scanned by FTIR spectroscopy, a new undefined, probably non-H-bonded, structure for tropoelastin produced by agLDL-VSMC is revealed. By differential scanning calorimetry, a decrease of water affinity and a drop of the glass transition associated with aggregated tropoelastin (from 200°C to 159°C) in the supernatant from agLDL VSMC are evidenced. This second phenomenon is due to an interaction between agLDL and tropoelastin as detected by the weak specific FTIR absorption band of agLDL in supernatant from agLDL-loaded VSMC. 1. Introduction VSMC in atherosclerotic lesion are unable to produce normal elastic fibers due to atherosclerotic risk factors such as diabetes and associated hyperglycemia, endothelial dysfunction, and inflammation [1, 2]. If experimental hypercholesterolemia decreases the wall elastin content in vivo [3] and in vitro systems [4], the role of hypercholesterolemia in the altered VSMC elastogenic capacity and the possible mechanisms involved are not yet elucidated. VSMC become foam cells through the uptake of diversely modified LDLs [5, 6], whereas the aggregation of LDLs (agLDL) seems to be a key condition for lipid accumulation in VSMCs [7, 8]. Intracellular cholesterol accumulation alters proteoglycan composition [9] and collagen assembly [10] in VSMC, but it is unknown whether intracellular lipid may change the physical characteristics of the tropoelastin synthesized by human VSMC. The aim of this work was to characterize agLDL as well as tropoelastin produced by agLDL-lipid-loaded human VSMC versus that produced by control VSMC using polymer characterization techniques that were previously shown to be efficient in checking the molecular architecture and chain dynamics of proteins [11, 12]. 2. Materials and Methods 2.1. Human VSMC Primary cultures of human VSMC were obtained from nonatherosclerotic areas of human coronary arteries from hearts explanted during heart transplantation at Hospital of Santa Creu i Sant Pau as previously described [5, 6]. Donors of the explanted hearts were men between 40 and 60 years old. Explants were incubated at 37°C in a humidified atmosphere of 5% CO2. Cells grown out of explants were suspended in a solution of trypsin/EDTA and
Identification of pro-angiogenic markers in blood vessels from stroked-affected brain tissue using laser-capture microdissection
Mark Slevin, Jerzy Krupinski, Norma Rovira, Marta Turu, Ana Luque, Maribel Baldellou, Coral Sanfeliu, Nuria de Vera, Lina Badimon
BMC Genomics , 2009, DOI: 10.1186/1471-2164-10-113
Abstract: Here, we have isolated active (CD105/Flt-1 positive) and inactive (CD105/Flt-1 minus (n=5) micro-vessel rich-regions from stroke-affected and contralateral tissue of patients using laser-capture micro-dissection. Areas were compared for pro- and anti-angiogenic gene expression using targeted TaqMan microfluidity cards containing 46 genes and real-time PCR. Further analysis of key gene de-regulation was performed by immunohistochemistry to define localization and expression patterns of identified markers and de novo synthesis by human brain microvessel endothelial cells (HBMEC) was examined following oxygen-glucose deprivation (OGD). Our data revealed that seven pro-angiogenic genes were notably up-regulated in CD105 positive microvessel rich regions. These were, beta-catenin, neural cell adhesion molecule (NRCAM), matrix metalloproteinase-2 (MMP-2), tissue inhibitor of matrix metalloproteinase-1 (TIMP-1), hepatocyte growth factor-alpha (HGF-alpha), monocyte chemottractant protein-1 (MCP-1) and and Tie-2 as well as c-kit. Immunohistochemistry demonstrated strong staining of MMP-2, HGF-alpha, MCP-1 and Tie-2 in stroke-associated regions of active remodeling in association with CD105 positive staining. In vitro, OGD stimulated production of Tie-2, MCP-1 and MMP-2 in HBMEC, demonstrated a de novo response to hypoxia.In this work we have identified concurrent activation of key angiogenic molecules associated with endothelial cell migration, differentiation and tube-formation, vessel stabilization and stem cell homing mechanisms in areas of revascularization. Therapeutic stimulation of these processes in all areas of damaged tissue might improve morbidity and mortality from stroke.Stroke is a leading cause of death and disability in the Western world. Neuronal survival in peri-infarcted regions determines the extent of patient recovery [1]. Patients with a higher density of blood vessels have reduced morbidity and mortality [2]. Restoration of cerebral microvascular circu
Angina, “Normal” Coronary Angiography, and Vascular Dysfunction: Risk Assessment Strategies
Raffaele Bugiardini ,Lina Badimon,Peter Collins,Raimund Erbel,Kim Fox,Christian Hamm,Fausto Pinto,Annika Rosengren,Christodoulos Stefanadis,Lars Wallentin,Frans Van de Werf
PLOS Medicine , 2007, DOI: 10.1371/journal.pmed.0040012
Alterations of specific biomarkers of metabolic pathways in vascular tree from patients with Type 2 diabetes
Bernal-Lopez M Rosa, Llorente-Cortes Vicenta, Gomez-Carrillo Victor, Lopez-Carmona Dolores, Calleja Fernando, Gomez-Huelgas Ricardo, Badimon Lina, Tinahones J
Cardiovascular Diabetology , 2012, DOI: 10.1186/1475-2840-11-86
Abstract: The atherosclerotic process in OPA from diabetic patients was associated with high expression levels of inflammatory, lipid metabolism and apoptotic biomarkers. The degree of glycemic control was associated with gene expression markers of apoptosis, lipid metabolism and antioxidants in FV. However, the effect of glycemic control on pro-atherosclerotic gene expression was very low in arteries with established atherosclerosis.Cardiovascular diseases (CVD) are highly prevalent in the general population, affecting most adults over 60?years of age. Vascular endothelium has unique responses to hemodynamic forces. The flow and hemodynamic forces are not uniform in the vascular system. The endothelium of the vascular circulation is exposed to hemodynamic forces of greater magnitude than in other human tissues. Hemodynamic forces play an important role in vascular diseases, especially in the location of atheromas [1].The pathophysiology of arterial thrombosis is different from that of venous thrombosis. In the arteries there is altered endothelium-platelet adhesion, greatly influenced by hemodynamic forces, while the major factors for venous thrombosis are the phenomena of slow or stagnant blood flow, combined with hypercoagulability situations [2].Sustained flow with high shear stress upregulates gene and then protein expression in endothelial cells, which has a protective effect against the atherosclerotic process [3]. In the venous system, a disturbed flow leads to inflammation and venous thrombosis, and therefore the development of chronic vessel disease, such as peripheral arterial disease.Atherosclerosis is associated with processes such as inflammation [4] lipid metabolism [5], apoptosis [6] and the immune system responses [5]. Epidemiologic studies show a consistent association between diabetes and cardiovascular disease [7]. The influence of evaluating the atherosclerosis process according to the effect of tight glycemic control has been less convincing in clinical
C-reactive protein exerts angiogenic effects on vascular endothelial cells and modulates associated signalling pathways and gene expression
Marta M Turu, Mark Slevin, Sabine Matou, David West, Cristina Rodríguez, Ana Luque, Marta Grau-Olivares, Lina Badimon, Jose Martinez-Gonzalez, Jerzy Krupinski
BMC Cell Biology , 2008, DOI: 10.1186/1471-2121-9-47
Abstract: Here, we show that CRP is a powerful inducer of angiogenesis in bovine aortic EC (BAEC) and human coronary artery EC (HCAEC). CRP, at concentrations corresponding to moderate/high risk (1–5 μg/ml), induced a significant increase in proliferation, migration and tube-like structure formation in vitro and stimulated blood vessel formation in the chick chorioallantoic membrane assay (CAM). CRP treated with detoxi-gel columns retained such effects. Western blotting showed that CRP increased activation of early response kinase-1/2 (ERK1/2), a key protein involved in EC mitogenesis. Furthermore, using TaqMan Low-density Arrays we identified key pro-angiogenic genes induced by CRP among them were vascular endothelial cell growth factor receptor-2 (VEGFR2/KDR), platelet-derived growth factor (PDGF-BB), notch family transcription factors (Notch1 and Notch3), cysteine-rich angiogenic inducer 61 (CYR61/CCN1) and inhibitor of DNA binding/differentiation-1 (ID1).This data suggests a role for CRP in direct stimulation of angiogenesis and therefore may be a mediator of neovessel formation in the intima of vulnerable plaques.Atherosclerosis is the underlying cause of ischemic cardiovascular and cerebrovascular diseases [1-3]. Unstable carotid atherosclerotic plaques can undergo thrombotic complications and trigger acute clinical events [4-6]. In atherosclerotic plaques angiogenesis allows the formation of new microvessels to maintain oxygen and nutrient supply for vascular cells. Such processes are potenciated by different molecules secreted by vascular and inflammatory cells [5]. Neovessel growth occurs in active regions of atherosclerotic lesions undergoing remodelling. Our previous studies have demonstrated specific molecular deregulation occurring in these regions, consistent with the promotion of angiogenesis. The new vessels of atherosclerotic lesions may be a focus of instability, since they facilitate the infiltration of inflammatory cells and due to their tendency to leak,
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