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2 edition of Role of vascular endothelial growth factor A in the glomerulus found in the catalog.

Role of vascular endothelial growth factor A in the glomerulus

Vera Eremina

Role of vascular endothelial growth factor A in the glomerulus

analysis of phenotypes with glomerular-specific alterations of VEGF-A expression in murine transgenic lines

by Vera Eremina

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Published .
Written in English


About the Edition

Vascular Endothelial Growth Factor A (VEGF-A) is a critical mediator of vasculogenesis and angiogenesis. It is required for the establishment and maintenance of endothelial fenestrae in-vitro. Knockouts of VEGF-A or its receptors in mice result in lethality at midgestation. These early lethal phenotypes preclude the analysis of the role of VEGF-A signaling in the kidney.In the thesis, the role of VEGF-A in the development and maintenance of the glomerular filtration barrier is presented based on data from the VEGF-A transgenic mouse lines generated during my doctoral studies.To fully understand the biologic role of VEGF-A in the glomerulus, the level of VEGF-A was manipulated in fully differentiated adult glomeruli. Cre-mediated VEGF-A deletion from glomeruli of adult mice led to renal-restricted thrombotic microangiopathy and subsequent glomerulosclerosis.The Cre-loxP conditional gene targeting system and a combination of hypomorphic and null VEGF-A alleles were used to alter the gene dose of VEGF-A produced by podocytes in transgenic mice. It was demonstrated in-vivo that each VEGF-A gene dose is associated with distinct clinical and pathological phenotypes in murine models. Podocyte-specific deletion of both VEGF-A alleles leads to congenital nephropathy and perinatal lethality. Mice with podocyte-specific haploinsufficiency for all VEGF-A isoforms develop glomerular endotheliosis, the renal lesion seen in preeclampsia. Further reduction of VEGF-A leads to mesangiolysis and end stage renal disease by 3 weeks of age. Podocyte-specific overexpression of the 164 isoform of VEGF-A results in collapsing glomerulopathy, the classic lesion seen in HIV-associated nephropathy.These results provide the first genetic evidence that endogenous VEGF-A production is required for maintenance of a differentiated vascular bed and more specifically for integrity of the glomerular filtration barrier. These findings may help to explain the observation that a subset of patients treated with VEGF-A inhibitors develop proteinuria.Dysregulation of VEGF-A expression has been identified in a wide variety of renal diseases. Conversely, infusion of VEGF-A into animals with thrombotic thrombocytopenic purpura, diabetic glomerulopathy or a remnant kidney appears to be protective.

Edition Notes

Statementby Vera Eremina.
The Physical Object
Paginationxiii, 187 leaves.
Number of Pages187
ID Numbers
Open LibraryOL19758184M
ISBN 109780494158708

ful, endothelial growth factor. It is a potent and powerful vascular per-meabilizing agent,27 and a potent vasodilator It increases migration of endothelial cells, new vessel formation,29 and has effects on the pericytes that surround endothelial cells,30 and on the matrix metal-loproteinases secreted by endothelial cells The net result. Several platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) family members display C-terminal protein motifs that confer retention of the secreted factors within the pericellular space. in defective investment of pericytes in the microvessel wall and delayed formation of the renal glomerulus mesangium. Long.

The vascular endothelial growth factor-A (VEGF) plays a crucial role in tumor angiogenesis. Through its primary receptor VEGFR-2, VEGF exerts the activity of a multitasking cytokine, which is able to stimulate endothelial cell survival, invasion and migration into surrounding tissues, proliferation, as well as vascular permeability and inflammation. The core components of VEGF signaling. Glomerular and peritubular capillary number, density, and endothelial cell proliferation were determined in aging (24 months; n = 9) and young (3 months; n = 8) rat kidneys and correlated with renal functional and structural changes and alterations in renal expression of vascular endothelial growth factor (VEGF) and thrombospondin-1 (TSP-1).

the lymphatic system. Lymphangiogenesis plays a vital role in tumour growth and systemic dissemination of different carcinomas [2]. Vascular endothelial growth factor C (VEGF-C) is regarded development of new anticancer therapies to prevent local invasion as lymphangiogenic growth factor that has been implicated in and metastatic spread of disease. Vascular endothelial growth factor-A (VEGF-A), dimeric glycoprotein, is a potent endothelial cell-specific mitogen which plays a key role in angiogenesis, especially in response to ischemia. Biomarkers reflect various pathophysiological faces of spherical LV transformation that related to myocardial stress due to persisted ischemia, fibrosis, and inflammation, and they may be helpful to.


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Role of vascular endothelial growth factor A in the glomerulus by Vera Eremina Download PDF EPUB FB2

Abstract Purpose of review Vascular endothelial growth factor is a major regulator of blood vessel biology and is highly expressed in presumptive and mature podocytes within the glomerulus. It has long been recognized that dysregulation of this factor occurs in a number of glomerular diseases; however, definitive proof that it plays a pathogenic or developmental role in glomerular biology has Cited by: BACKGROUND/AIMS: Vascular endothelial growth factor is a major regulator of angiogenesis and vascular permeability [Carmeliet et al.: Nature ;].

The podocyte, the outermost layer of the glomerular filtration barrier, produces large amounts of by: Over a decade and a half has passed since the publication of early reports hinting at a pathogenetic role for vascular endothelial growth factor ("VEGF") in the development of diabetic kidney disease.

In diabetic rats, renal mRNA levels of the VEGF-A isoform were upregulated and administration of a. The vascular endothelial growth factor (VEGF) family of proteins are key regulators of physiological systems. Originally linked with endothelial function, they have since become understood to be. Based on the recent advancement, this review revisits comprehensive morphological development of the glomerulus.

Recent findings: Interactions of presumptive podocyte vascular endothelial growth factor with vascular endothelial growth factor-2 on angioblasts initiate glomerular vascularization. In induced pluripotent stem cells or organoid Author: Michio Nagata.

Role of vascular endothelial growth factor in diabetic nephropathy. Background. Vascular endothelial growth factor (VEGF) is a potent cytokine that is considered to be an important mediator in the pathogenesis of endothelial dysfunction in diabetes.

Even though VEGF staining in the glomerulus decreased with worsening of diabetic nephropathy. Vascular endothelial growth factor-A (VEGF) is required for endothelial cell differentiation and physiological role of the glomerulus is to allow the flow of fluid into the urinary space of the Bowman’s capsule, but prevent the passage of blood proteins, such as albumin, into the urine.

PURPOSE OF REVIEW: Vascular endothelial growth factor is a major regulator of blood vessel biology and is highly expressed in presumptive and mature podocytes within the glomerulus. It has long been recognized that dysregulation of this factor occurs in a number of glomerular diseases; however, definitive proof that it plays a pathogenic or.

Aside from being part of the filtration barrier, podocytes also help maintain the shape of the capillary loop shape by counteracting intraglomerular pressure. Lastly, podocytes produce vascular endothelial growth factor (VEGF) to which is a molecule that the glomerular endothelial cell needs to survive.

Additional structures of the glomerulus. New blood vessel formation (angiogenesis) is a fundamental event in the process of tumor growth and metastatic dissemination. Hence, the molecular basis of tumor angiogenesis has been of keen interest in the field of cancer research.

The vascular endothelial growth factor (VEGF) pathway is well established as one of the key regulators of this process. The VEGF/VEGF-receptor axis is. W.M. Maniscalco, C.T. D’Angio, in Encyclopedia of Respiratory Medicine, Vascular endothelial growth factor (VEGF or VEGF-A) is the prototype and best-described member of a family of at least six largely endothelial-specific, heparin-binding, angiogenic growth factors.

VEGF family members are crucial to the normal development and maintenance of the vascular and lymphatic systems. Abstract: Vascular endothelial growth factor (VEGF) is a main regulator of blood vessel growth and plays an important role in promoting endothelial survival and maintaining the microvasculature.

The kidney is a highly vascularized organ and has two important microvasculatures; glomerular and peritubular capillaries. Vascular endothelial growth factor (VEGF), originally known as vascular permeability factor (VPF), is a signal protein produced by cells that stimulates the formation of blood vessels.

To be specific, VEGF is a sub-family of growth factors, the platelet-derived growth factor family of cystine-knot growth factors.

They are important signaling proteins involved in both vasculogenesis (the de. Vascular endothelial growth factor (VEGF) plays a major pathophysiological role in diabetic nephropathy, 12, 13 despite VEGF exhibiting protective roles in nondiabetic renal disease.

14, Vascular endothelial growth factor attenuates leukocyte-endothelium interaction during acute endothelial dysfunction: essential role of endothelium-derived nitric oxide. FASEB J. ; – Crossref Medline Google Scholar; Walshe TE, Dole VS, Maharaj AS, Patten IS, Wagner DD, D’Amore PA.

Vascular endothelial growth factor (VEGF) is constitutively expressed in the glomerulus where it may have a role in the maintenance of capillary endothelial cell integrity. The present study sought to examine changes in VEGF expression in a model of progressive renal disease and to assess the effects of angiotensin converting enzyme (ACE.

During quiescence, the “angiogenic switch” is “off”. However, during tumour development pro-angiogenic factors such as vascular endothelial growth factor (VEGF), basic and acidic fibroblast growth factor, tumour necrosis factor-α and interleukin-1 are pathologically enhanced.

The role of vascular endothelial growth factor (VEGF) in renal pathophysiology. Vascular endothelial growth factor (VEGF) istence of a paracrine loop in the glomerulus, VEGF must move in the opposite direction of the glomerular filtrate in order to bind to its receptors. The presence. The glomerulus is a highly specialized microvascular bed that filters blood to form primary urinary filtrate.

It contains four cell types: fenestrated endothelial cells, specialized vascular support cells termed podocytes, perivascular mesangial cells, and parietal epithelial cells.

Glomerular cell-cell communication is critical for the development and maintenance of the glomerular filtration.

A glomerulus is formed by growth of Bowman's capsule harmonized with a capillary during kidney development. The vascular endothelial growth factor (VEGF) is an essential angiogenic cytokine, and VEGF deficiency is known to be fatal in mice in early embryonic stages.

Ang1: Angiopoietins are a family of endothelial cell growth factors, with essential roles in regulating vascular growth, development and maturation. The complex interaction between the angiopoietins and vascular endothelial growth factors determine endothelial cell behaviour, therefore they are key players in microvascular permeability, both in.Cell viability and expression of specific proteins (nephrin, synaptopodin, vascular endothelial growth factor receptor 2 (VEGFR2) and von Willebrandt factor (vWF)) were maintained for 19 days in.Vascular endothelial growth factor (VEGF) plays a crucial role in developmental and pathological angiogenesis.

Expression of VEGF in quiescent adult tissue suggests a potential role in the maintenance of mature blood vessels. We demonstrate, using a Vegf–lacZ reporter mouse model, that VEGF is expressed by arterial but not by venous or capillary endothelial cells (ECs) in vivo.