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VEGF Gene Expression (vegf + gene_expression)
Selected AbstractsVEGF GENE EXPRESSION IN PROTEINURIC RATSNEPHROLOGY, Issue 1 2002Kelly Dj [source] Vascular endothelial growth factor prevents G93A-SOD1-induced motor neuron degenerationDEVELOPMENTAL NEUROBIOLOGY, Issue 13 2009J. Simon Lunn Abstract Amyotrophic lateral sclerosis (ALS) is an adult-onset neurodegenerative disorder characterized by selective loss of motor neurons (MNs). Twenty percent of familial ALS cases are associated with mutations in Cu2+/Zn2+ superoxide dismutase (SOD1). To specifically understand the cellular mechanisms underlying mutant SOD1 toxicity, we have established an in vitro model of ALS using rat primary MN cultures transfected with an adenoviral vector encoding a mutant SOD1, G93A-SOD1. Transfected cells undergo axonal degeneration and alterations in biochemical responses characteristic of cell death such as activation of caspase-3. Vascular endothelial growth factor (VEGF) is an angiogenic and neuroprotective growth factor that can increase axonal outgrowth, block neuronal apoptosis, and promote neurogenesis. Decreased VEGF gene expression in mice results in a phenotype similar to that seen in patients with ALS, thus linking loss of VEGF to the pathogenesis of MN degeneration. Decreased neurotrophic signals prior to and during disease progression may increase MN susceptibility to mutant SOD1-induced toxicity. In this study, we demonstrate a decrease in VEGF and VEGFR2 levels in the spinal cord of G93A-SOD1 ALS mice. Furthermore, in isolated MN cultures, VEGF alleviates the effects of G93A-SOD1 toxicity and neuroprotection involves phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling. Overall, these studies validate the usefulness of VEGF as a potential therapeutic factor for the treatment of ALS and give valuable insight into the responsible signaling pathways and mechanisms involved. © 2009 Wiley Periodicals, Inc. Develop Neurobiol, 2009 [source] Vascular endothelial growth factor and diabetic retinopathy: pathophysiological mechanisms and treatment perspectivesDIABETES/METABOLISM: RESEARCH AND REVIEWS, Issue 6 2003Ruth B. Caldwell Abstract Retinal neovascularization and macular edema are central features of diabetic retinopathy, the major cause of blindness in the developed world. Current treatments are limited in their efficacy and are associated with significant adverse effects. Characterization of the molecular and cellular processes involved in vascular growth and permeability has led to the recognition that the angiogenic growth factor and vascular permeability factor vascular endothelial growth factor (VEGF) plays a pivotal role in the retinal microvascular complications of diabetes. Therefore, VEGF represents an exciting target for therapeutic intervention in diabetic retinopathy. This review highlights the current understanding of the mechanisms that regulate VEGF gene expression and mediate its biological effects and how these processes may become altered during diabetes. The cellular and molecular alterations that characterize experimental models of diabetes are considered in relation to the influence of high glucose-mediated oxidative stress on VEGF expression and on the mechanisms of VEGF's actions under hyperglycemic induction. Finally, potential therapeutic strategies for preventing VEGF overexpression or blocking its pathological effects in the diabetic retina are considered. Copyright © 2003 John Wiley & Sons, Ltd. [source] Increased expression of VEGF following exercise training in patients with heart failureEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2001T. Gustafsson Background and aims During the last decades several angiogenic factors have been characterized but so far it is unknown whether local muscle exercise training increases the expression of these factors in patients with moderate heart failure. Expression of the major putative angiogenic factor vascular endothelial growth factor (VEGF) at the level of messneger RNA (mRNA) and/or protein was therefore studied before and after 8 weeks of training in patient with chronic heart failure. Methods VEGF mRNA and protein concentrations were determined in skeletal muscle biopsies before and after 8 weeks of one-legged knee extension training in patients with chronic heart failure (New York Heart Association II,III). Results Exercise training increased the citrate synthase activity and peripheral exercise capacity by 46% and 36%, respectively, in parallel with a two-fold increase in VEGF at both the mRNA (P = 0·03) and protein (P = 0·02) levels Conclusion The increase in VEGF gene expression in response to exercise training indicates VEGF to be one possible mediator in exercise-induced angiogenesis and may therefore regulate an important and early step in adaptation to increased muscle activity in patient with chronic heart failure. [source] Induction of vascular endothelial growth factor expression in human pulp fibroblasts stimulated with black-pigmented BacteroidesINTERNATIONAL ENDODONTIC JOURNAL, Issue 9 2004L.-C. Yang Abstract Aim, To investigate the effect of black-pigmented Bacteroides on the expression of vascular endothelial growth factor (VEGF) gene in human pulp fibroblasts. Methodology, The supernatants of Porphyromonas endodontalis, Porphyromonas gingivalis and Prevotella intermedia were used to evaluate VEGF gene expression in human pulp fibroblasts. The levels of mRNAs were measured by the quantitative reverse-transcriptase polymerase chain reaction analysis. Results, Black-pigmented Bacteroides induced significantly high levels of VEGF mRNA gene expression in human pulp fibroblasts (P < 0.05). In addition, the expression of VEGF depended on the bacteria tested. Conclusions, Black-pigmented Bacteroides may be involved in developing pulpal disease through the stimulation of VEGF production that would lead to the expansion of the vascular network coincident to progression of the inflammation. [source] Expression of vascular endothelial growth factor in renal cell carcinoma is correlated with cancer advancementJOURNAL OF CLINICAL LABORATORY ANALYSIS, Issue 3 2003Ching-Chiang Yang Abstract Vascular endothelial growth factor (VEGF) functions as a regulator of neovascularization in malignant cells. VEGF as a mitogen is thought to alter renal cell carcinoma formation and tumor progression. We investigated the expression of the VEGF gene in order to evaluate its clinical significance in renal cell carcinoma. Tissue samples from 198 patients with renal cell carcinoma were examined with an immunohistochemical stain for the expression of the VEGF gene. The expression rate was compared to 34 normal renal cortical samples obtained from renal surgery from noncancer patients. There were significant differences between normal renal cortex (0%) and cancer tissue (54.5%) in positive staining of VEGF protein (P<0.001). With the progression of tumor grade, the positive rate of VEGF gene expression significantly increased. The expression rate of the VEGF gene in the advanced group, such as with lymph node involvement or vein invasion, was greater than that in the locally confined group (P<0.001). The results revealed that expression of the VEGF gene is proportional to the formation and progression of renal cell carcinoma, which may allow VEGF to be used as a prognostic marker for renal cell carcinoma. J. Clin. Lab. Anal. 17:85,89, 2003. © 2003 Wiley-Liss, Inc. [source] Shwachman,Diamond syndrome: an inherited model of aplastic anaemia with accelerated angiogenesisBRITISH JOURNAL OF HAEMATOLOGY, Issue 5 2006Elaine W. Leung Summary Bone marrow angiogenesis is increased in myelodysplastic syndromes (MDS) and acute myeloid leukaemia (AML), but has not been studied in inherited or acquired marrow failure syndromes. Shwachman,Diamond syndrome (SDS) carries a high risk of MDS/AML and is characterised by marrow stromal dysfunction. Compared with controls, SDS patients without MDS/AML had higher marrow microvessel density. Stromal VEGF gene expression, stromal vascular endothelial growth factor (VEGF) secretion and VEGF levels in serum and marrow mononuclear cells were normal. Future studies should investigate the mechanism for increased angiogenesis in SDS, and whether SDS marrow, with its increased angiogenesis, promotes progression of malignant clones. [source] 3- O -Methylfunicone, a metabolite produced by Penicillium pinophilum, modulates ERK1/2 activity, affecting cell motility of human mesothelioma cellsCELL PROLIFERATION, Issue 2 2010E. Buommino Objectives:, 3- O -methylfunicone (OMF), a secondary metabolite produced by Penicillium pinophilum, affects cell proliferation and motility in a variety of human solid tumours. The aim of this study was to demonstrate whether OMF has the ability to arrest cell division and motility, in a human mesothelioma cell line. Malignant mesothelioma is an aggressive cancer that does not respond to standard therapies the cells of which are considered to be highly resistant to apoptosis. Material and methods:, Cell motility and invasion were measured using a modified Boyden chamber. Gene expression was examined by RT-PCR, while ERK1/2 was investigated by Western blot analysis. All experiments were also performed on primary cultures of mesothelial cells. Results:, The present study shows that OMF inhibited motility of the NCI mesothelioma cell line by modulating ERK signalling activity, and affected ,V,5 integrin and MMP-2 expression, inducing marked downregulation at both mRNA and protein levels. Substantial downregulation of VEGF gene expression was also demonstrated. These effects were not observed in normal mesothelial cell cultures. Conclusion:, OMF may have potential as a naturally derived anti-tumour drug for treatment of mesothelioma. [source] Toluene diisocyanate enhances human bronchial epithelial cells' permeability partly through the vascular endothelial growth factor pathwayCLINICAL & EXPERIMENTAL ALLERGY, Issue 10 2009H. Zhao Summary Background Toluene diisocyanate (TDI) is a recognized chemical asthmogen; yet, the mechanisms of its toxicity have not been elucidated. Objective To investigate the influence of TDI on the permeability of human bronchial epithelial cell (HBE; HBE135-E6E7) monolayers in vitro, and the expression of vascular endothelial growth factor (VEGF) in these cells. Methods TDI,human serum albumin (HSA) conjugates were prepared by a modification of Son's method. Fluorescein isothiocyanate-labelled dextran and transmission electron microscopy were used to evaluate the effects of TDI,HSA on HBE135-E6E7 permeability. RT-PCR and ELISA were used to evaluate VEGF gene expression and protein release from HBE135-E6E7 cells stimulated by TDI,HSA. A VEGF-neutralizing antibody was used in monolayer permeability experiments to determine the role of the VEGF pathway in this process. Results TDI,HSA significantly increased the permeability coefficients of HBE135-E6E7 monolayers (P<0.01). TDI,HSA treatment significantly increased the expression of VEGF165 and VEGF189 genes (P<0.01). ELISA showed that TDI significantly induces VEGF release from HBE135-E6E7 cells. Cells treated with TDI,HSA and VEGF-neutralizing antibody had significantly lower permeability coefficients than cells treated with TDI,HSA only (P<0.01), but still significantly higher than control cells (P<0.01). Cells treated with TDI,HSA had fewer tight junctions (TJs) than control and HSA-treated cells, and addition of the anti-VEGF antibody did not restore the original number of TJs. Conclusion TDI increases the permeability of HBE cell monolayers, partly through a VEGF-mediated pathway. This suggests the importance of VEGF in TDI-induced pulmonary diseases, but shows that other pathways may be involved in the pathogenic process. [source] | |||||||||||||