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Vascular Defects (vascular + defect)
Selected AbstractsOcular perfusion and age-related macular degenerationACTA OPHTHALMOLOGICA, Issue 2 2001Thomas A. Ciulla ABSTRACT. Purpose: To review the role of ocular perfusion in the pathophysiology of age-related macular degeneration (AMD), the leading cause of irreversible blindness in the industrialized world. Methods: Medline search of the literature published in English or with English abstracts from 1966 to 2000 was performed using various combinations of relevant key words. Results: Vascular defects have been identified in both nonexudative and exudative AMD patients using fluorescein angiographic methods, laser Doppler flowmetry, indocyanine green angiography, and color Doppler imaging. Conclusion: Although these studies lend some support to the vascular pathogenesis of AMD, it is not possible to determine if the choroidal perfusion abnormalities play a causative role in nonexudative AMD, if they are simply an association with another primary alteration, such as a primary RPE defect or a genetic defect at the photoreceptor level, or if they are more strongly associated with one particular form of this heterogeneous disease. Further study is warranted. [source] Zebrafish notch signalling pathway mutants exhibit trunk vessel patterning anomalies that are secondary to somite misregulationDEVELOPMENTAL DYNAMICS, Issue 10 2010Christina Therapontos Abstract The Notch signalling pathway mutants, after-eight (aei), beamter (bea), and deadly-seven (des) have previously been used to study somitogenesis and neurogenesis. Notch signalling has also been shown to have roles in vascular development. However, vascular development in each of these three Notch mutants has not been described, and so their potential usefulness for further understanding the role of Notch signalling in angiogenesis is unknown. Here we demonstrate each of the mutants also exhibit vascular defects in inter-somitic vessel (ISV) positioning and patterning. Ectopic filopodia were also observed on the ISVs of the mutants. Ectopic filopodia are not due to loss of dll4. Somite expression of known vascular guidance cues, efnb2, sema3a2, and plexinD1 are disrupted, suggesting that the ISV vascular phenotype is due to disruption of these cues. Developmental Dynamics 239:2761,2768, 2010. © 2010 Wiley-Liss, Inc. [source] Role of VEGF and tissue hypoxia in patterning of neural and vascular cells recruited to the embryonic heartDEVELOPMENTAL DYNAMICS, Issue 11 2009Hongbin Liu Abstract We hypothesized that oxygen gradients and hypoxia-responsive signaling may play a role in the patterning of neural or vascular cells recruited to the developing heart. Endothelial progenitor and neural cells are recruited to and form branched structures adjacent to the relatively hypoxic outflow tract (OFT) myocardium from stages 27,32 (ED6.5,7.5) of chick development. As determined by whole mount confocal microscopy, the neural and vascular structures were not anatomically associated. Adenoviral delivery of a VEGF trap dramatically affected the remodeling of the vascular plexus into a coronary tree while neuronal branching was normal. Both neuronal and vascular branching was diminished in the hearts of embryos incubated under hyperoxic conditions. Quantitative analysis of the vascular defects using our recently developed VESGEN program demonstrated reduced small vessel branching and increased vessel diameters. We propose that vascular and neural patterning in the developing heart share dependence on tissue oxygen gradients but are not interdependent. Developmental Dynamics 238:2760,2769, 2009. © 2009 Wiley-Liss, Inc. [source] Obesity, Insulin Resistance, and Capillary RecruitmentMICROCIRCULATION, Issue 4-5 2007Stephen Rattigan ABSTRACT Objective: Insulin has vascular actions within the skeletal muscle microcirculation (capillary recruitment) that enhance its own access and that of glucose to the muscle cells. Obesity and insulin resistance are associated with dysregulated vascular function within muscle and a loss of insulin-mediated capillary recruitment. Furthermore, agents that impair insulin's vascular actions to recruit capillaries lead to acute insulin resistance in terms of muscle glucose uptake. Together these data suggest a strong connection between the loss of insulin-mediated capillary recruitment and the development of insulin resistance. This review examines the mechanisms involved in insulin-mediated capillary recruitment and the vascular defects associated with obesity and insulin resistance that may impair the capillary recruiting process. Understanding the mechanisms of insulin-mediated capillary recruitment and its impairment may lead to new treatment avenues to prevent the progression of obesity to diabetes. [source] Antiangiogenic plasma activity in patients with systemic sclerosisARTHRITIS & RHEUMATISM, Issue 10 2007Mary Jo Mulligan-Kehoe Objective Systemic sclerosis (SSc; scleroderma) is a systemic connective tissue disease with an extensive vascular component that includes aberrant microvasculature and impaired wound healing. The aim of this study was to investigate the presence of antiangiogenic factors in patients with SSc. Methods Plasma samples were obtained from 30 patients with SSc and from 10 control patients without SSc. The samples were analyzed for the ability of plasma to affect endothelial cell migration and vascular structure formation and for the presence of antiangiogenic activity. Results Exposure of normal human microvascular dermal endothelial cells to plasma from patients with SSc resulted in decreased cell migration (mean ± SEM 52 ± 5%) and tube formation (34 ± 6%) compared with that in plasma from control patients (P < 0.001 for both). SSc plasma contained 2.9-fold more plasminogen kringle 1,3 fragments (angiostatin) than that in control plasma. The addition of angiostatin to control plasma resulted in inhibition of endothelial cell migration and proliferation similar to that observed in SSc plasma. In vitro studies demonstrated that granzyme B and other proteases contained in T cell granule content cleave plasminogen and plasmin into angiostatin fragments. Conclusion Plasminogen conformation in patients with SSc enables granzyme B and granule content protease to limit the proangiogenic effects of plasmin and increase the levels of antiangiogenic angiostatin. This increase in angiostatin production may account for some of the vascular defects observed in patients with SSc. [source] | ||||||||||