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| Author | : Hamid Massaeli |
| Publisher | : |
| Total Pages | : 0 |
| Release | : 2000 |
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| Release | : 1902 |
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Low density lipoprotein (LDL) is an important risk factor for atherosclerotic disease. LDL may be oxidized (oxLDL) by free radicals in a lipid and an aqueous environment. OxLDL plays an important role in atherosclerosis, possibly by altering Ca2+ within vascular smooth muscle cells (VSMC). Acute exposure of VSMC to oxLDL immediately increased [Ca2+] i through an IP3 mediated pathway. However, atherosclerosis is a gradual process in which VSMCs are more likely exposed to low concentrations of oxLDL over extended periods of time rather than acute exposures. It is very possible, therefore, that lower [oxLDL] and longer exposure times may induce a very different response with regard to regulation of [Ca2+]i. VSMC incubated with oxLDL (0.001-0.025 mg/ml) for up to 6 days significantly decreased [Ca2+]i transients in response to a variety of inotropic agents. OxLDL did not have a cytotoxic effect. Therefore, we hypothesized that a disruption in the IP 3 or ryanodine dependent release of SR Ca2+ may be the mechanism responsible for this effect. As detected by immunocytochemical analysis chronic exposure of VSMC to oxLDL induced a depression in the density of both IP3 and ryanodine receptors. This trend was also observed in aortic sections from rabbits maintained on a high cholesterol diet. Similar treatment conditions significantly increased the total SERCA2 ATPase content. At higher [oxLDL], we observed a significant loss of myosin and actin as the cell phenotype changed. In addition, these proteins formed giant aggregates which appeared to be in the process of being expelled from the cell. Our data demonstrate, therefore, that the change in Ca2+i is very different depending upon prior exposure of VSMC to oxLDL. The two effects of oxLDL on Ca2+i may play very different but equally important pathogenic roles in atherosclerosis. The acute effects may play an important pathogenic role in the initial atherosclerotic process, the chronic effects of oxLDL may provide a mechani.
| Author | : Michel Félétou |
| Publisher | : Morgan & Claypool Publishers |
| Total Pages | : 309 |
| Release | : 2011 |
| Genre | : Science |
| ISBN | : 1615041230 |
The endothelium, a monolayer of endothelial cells, constitutes the inner cellular lining of the blood vessels (arteries, veins and capillaries) and the lymphatic system, and therefore is in direct contact with the blood/lymph and the circulating cells. The endothelium is a major player in the control of blood fluidity, platelet aggregation and vascular tone, a major actor in the regulation of immunology, inflammation and angiogenesis, and an important metabolizing and an endocrine organ. Endothelial cells controls vascular tone, and thereby blood flow, by synthesizing and releasing relaxing and contracting factors such as nitric oxide, metabolites of arachidonic acid via the cyclooxygenases, lipoxygenases and cytochrome P450 pathways, various peptides (endothelin, urotensin, CNP, adrenomedullin, etc.), adenosine, purines, reactive oxygen species and so on. Additionally, endothelial ectoenzymes are required steps in the generation of vasoactive hormones such as angiotensin II. An endothelial dysfunction linked to an imbalance in the synthesis and/or the release of these various endothelial factors may explain the initiation of cardiovascular pathologies (from hypertension to atherosclerosis) or their development and perpetuation. Table of Contents: Introduction / Multiple Functions of the Endothelial Cells / Calcium Signaling in Vascular Cells and Cell-to-Cell Communications / Endothelium-Dependent Regulation of Vascular Tone / Conclusion / References
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| Release | : 2001 |
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| Author | : Protasio L. Da Luz |
| Publisher | : Academic Press |
| Total Pages | : 760 |
| Release | : 2018-02-03 |
| Genre | : Medical |
| ISBN | : 0128125519 |
Endothelium and Cardiovascular Diseases: Vascular Biology and Clinical Syndromes provides an in-depth examination of the role of endothelium and endothelial dysfunction in normal vascular function, and in a broad spectrum of clinical syndromes, from atherosclerosis, to cognitive disturbances and eclampsia. The endothelium is a major participant in the pathophysiology of diseases, such as atherosclerosis, diabetes and hypertension, and these entities are responsible for the largest part of cardiovascular mortality and morbidly. Over the last decade major new discoveries and concepts involving the endothelium have come to light. This important reference collects this data in an easy to reference resource. Written by known experts, and covering all aspects of endothelial function in health and disease, this reference represents an assembly of recent knowledge that is essential to both basic investigators and clinicians. Provides a complete overview of endothelial function in health and diseases, along with an assessment of new information Includes coverage of groundbreaking areas, including the artificial LDL particle, the development of a new anti-erectile dysfunction agent, a vaccine for atherosclerosis, coronary calcification associated with red wine, and the interplay of endoplasmic reticulum/oxidative stress Explores the genetic features of endothelium and the interaction between basic knowledge and clinical syndromes
| Author | : Roberta Lugano |
| Publisher | : |
| Total Pages | : 235 |
| Release | : 2013 |
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High levels of circulating low-density lipoproteins (LDL) are one of the major cardiovascular risk factors. Hypercholesterolemia induces endothelial dysfunction and chronic intimal inflammatory cell accumulation, hallmarks of the initiation of atherosclerosis. Additionally, growing human atherosclerotic plaques show proliferation and migration of vascular smooth muscle cells (VSMC) towards the intima producing remodeling of the vascular wall. However, those plaques that are most prone to rupture show a progressive loss of VSMC becoming soft and vulnerable and these lipid-rich high risk plaques cause clinical episodes resulting in morbid or fatal ischemic events. The mechanisms involved in the transformation of a plaque into a vulnerable VSMC-depleted atheroma have not been completely elucidated. Lipid-rich-VSMC have an impaired vascular repair function due to changes in cytoskeleton proteins. However, the effects of LDL on VSMC function during plaque remodeling and vascular repair are not fully understood. Thus, the aim of this thesis was to investigate early changes directly induced by LDL on VSMC phenotype and function and to identify the molecular mechanisms involved. This thesis demonstrates that the cardiovascular risk of hypercholesterolemia involves the interaction of LDL with VSMC and the regulation at a molecular level of different pathways that converge in the cell's migratory capacity. Migratory function of lipid-loaded VSMC can be restored by inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG-CoA) through a Rho kinase and myosin light chain phosphatase dependent mechanism. In addition, the studies performed in this thesis show that LDL affect VSMC adhesion, migration and cytoskeleton dynamics through the abrogation of the urokinase-plasminogen activator (uPA)/uPA receptor (uPAR) system function and by modulation of HSP27 phosphorylation and subcellular localization.
| Author | : John F. Keaney Jr. |
| Publisher | : Springer Science & Business Media |
| Total Pages | : 404 |
| Release | : 1999-12-31 |
| Genre | : Medical |
| ISBN | : 9780792386780 |
One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.
| Author | : Christie M. Ballantyne |
| Publisher | : Elsevier Health Sciences |
| Total Pages | : 605 |
| Release | : 2009-01-01 |
| Genre | : Medical |
| ISBN | : 1416054693 |
Clinical Lipidology, a companion to Braunwald's Heart Disease, is designed to guide you through the ever-changing therapeutic management of patients with high cholesterol levels. From basic science to pathogenesis of atherothrombotic disease, to risk assessment and the latest therapy options, this medical reference book offers unparalleled coverage and expert guidance on lipidology in a straightforward, accessible, and user-friendly style. Get authoritative guidance from some of the foremost experts in the field. Easily access key content with help from treatment algorithms. Access options and evidence-based solutions for every type of patient scenario, as well as the latest clinical guidelines and clinically relevant evidence on risk assessment, special patient populations, and therapy, including recently approved and experimental therapies. Remain at the forefront of the cardiology field with up-to-date chapters on treatment guidelines; diet, exercise, and weight loss; pharmacologic therapies such as statins, omega-3 fatty acids, and combination therapy; evolving targets of therapy such as PCSK9 inhibition, CETP inhibition, and inflammation Prepare for special patient populations such as children and adolescents; women and the elderly; transplant recipients; HIV patients; and those with chronic renal disease, familial hypercholesterolemia, other severe hypercholesterolemias, diabetes, or other metabolic syndromes. Take advantage of a format that follows that of the well-known and internationally recognized Braunwald's Heart Disease. Expert Consult eBook version included with purchase.
| Author | : Rao M. Uppu |
| Publisher | : Humana Press |
| Total Pages | : 480 |
| Release | : 2012-04-06 |
| Genre | : Science |
| ISBN | : 9781617796838 |
This cutting-edge and updated book offers methods for the rapid detection of RONs and redox stress. It includes in-depth analysis of natural and synthetic antioxidants, and also of DNA oxidation, oxidative lipidomics, and biomarkers.
| Author | : |
| Publisher | : Elsevier |
| Total Pages | : 427 |
| Release | : 1995-10-24 |
| Genre | : Science |
| ISBN | : 0080543502 |
In the last several years, the development of reagents that recognize smooth muscle-specific proteins has enabled researchers to identify smooth muscle cells (SMC) in tissue undergoing both differentiation and repair. These developments have led to increased research on SMC. The latest volume in the Biology of the Extracellular Matrix Series takes a current and all-encompassing look at this growing area of research. Devoted entirely to the subject of SMC, the book covers a diversity of topics-from SMC architecture and contractility to differentiation and gene expression in development. It also examines the proliferation and replication of SMC and its role in pharmacology and vascular disease. A must for cell, developmental, and molecular biologists, this book also will appeal to cardiologists, pathologists, and biomedical researchers interested in smooth muscle cells. Presents a molecular, genetic, and developmental perspective of the vas smooth muscle cell Overview sections highlight key points of chapters, including the clinical relevance of the research and expectations for future study Appeals to both the basic biologist and to the biomedical researcher of vascular disease
