HUGO ID Detailed Result 12680


HUGO ID 12680
Symbol VEGFA
Name vascular endothelial growth factor A
#Occurrence 93
#Paper 4

 


PMID Match String Actual String Score Flanking text Edited by Edit
12654515VEGFVEGF4.3Vascular endothelial growth factor (VEGF) VEGF is neurotrophic and also protects from hypoxia-induced neuronal injury 
12654515VEGFVEGF4.3The potential role of VEGF in preventing mutant SOD1-mediated motor neuron cell death was examined 
12654515VEGFVEGF4.3However NSC34 cells pretreated with VEGF displayed a dose-dependent resistance to oxidative damage from hydrogen peroxide 
12654515VEGFVEGF4.3VEGF activated both PI3-K and MAPK activities in mouse NSC34 motor 
12654515VEGFVEGF4.3of MAPK and PI3-K revealed that the protective effects of VEGF were mediated via the PI3-K activity and that MAPK activation 
12654515VEGFVEGF-induced3.8Furthermore VEGF-induced downstream Akt activation promoted motor neuron-like NSC34 cell survival in 
12654515VEGFVEGF4.3Thus VEGF protected mouse NSC34 motor neuron-like cell death from mutant G93A-SOD1 
12654515VEGFVEGF4.3Recently vascular endothelial growth factor (VEGF) VEGF has been demonstrated to have neurotrophic effects by promoting neuronal 
12654515VEGFVEGF4.3Knockout mice with deleted hypoxic response elements in the VEGF promoter region develop a motor neuron-like disease mimicking human ALS 
12654515VEGFVEGF4.3motor neuron-like disease mimicking human ALS 40 suggesting that hypoxia-mediated VEGF expression may be associated with motor neuron degeneration 
12654515VEGFVEGF4.3VEGF also known as vascular permeability factor is a dimeric glycoprotein 
12654515VEGFVEGF4.3Acting through these receptors VEGF is believed to initiate several intracellular signal transduction systems including 
12654515VEGFVEGF4.3Hypoxia and spinal cord injury have been demonstrated to increase VEGF expression 19 20 and 35 
12654515VEGFVEGF4.3Neuronal or neuronal-like cells pretreated with VEGF prevent glutamate- and hypoxia/ischemia-mediated hypoxia ischemia-mediated cell death in vitro 
12654515VEGFVEGF4.3More importantly topical application of VEGF reduces ischemia-mediated brain damage in vivo 19 
12654515VEGFVEGF4.3Although some studies have focused on the effects of VEGF on the central nervous system (CNS), CNS the potential role 
12654515VEGFVEGF4.3the central nervous system (CNS), CNS the potential role of VEGF in motor neuron survival by mutant SOD1 effects remains largely 
12654515VEGFVEGF4.3the NSC34 motor neuron-like cell culture model to test whether VEGF can prevent mutant SOD1-mediated motor neuron degeneration 
12654515VEGFVEGF4.3causes severe disease onset and progression was used to analyze VEGF effects on motor neuron degeneration 
12654515VEGFVEGF4.3We demonstrate that NSC34 cells pretreated with VEGF reduces mutant G93A-SOD1- TNF-_amp_#x3b1;- and hydrogen peroxide-mediated motor neuron-like cell 
12654515VEGFVEGF4.3VEGF activates both PI3-K and MAPK activities in NSC34 motor neuron-like 
12654515VEGFVEGF4.3Thus we propose that the neurotrophic-like activity of VEGF on mouse NSC34 motor neuron-like cell survival is mediated by 
12654515VEGFVEGF4.3VEGF was purchased from Calbiochem (San San Diego CA USA 
12654515VEGFVEGF4.3Mouse NSC34 cells were pretreated with VEGF for 30 min and then infected with 2_amp_#xd7 10 6 
12654515VEGFVEGF4.3with complete medium either in the presence or absence of VEGF for various lengths of time before analysis 32 2.5 
12654515VEGFVEGF-stimulated3.8Briefly control and VEGF-stimulated NSC34 cells were washed twice with ice-cold PBS and lysed 
12654515VEGFVEGF-treated3.8expressed as mean_amp_#xb1 S.E.M and the differences between vehicle- and VEGF-treated mouse NSC34 motor neuron-like cells were analyzed using two-tailed Student 
12654515VEGFVEGF4.3VEGF protects from mutant SOD1- TNF-_amp_#x3b1;- and H 2 O 2 
12654515VEGFVEGF4.3VEGF and vehicle pretreated mouse NSC34 cells were infected with adenovirus 
12654515VEGFVEGF4.3VEGF treatment was associated with significant increases in cell survival in 
12654515VEGFVEGF4.3VEGF transiently activates PI3-K and MAPK activities 
12654515VEGFVEGF4.3Thus we tested whether VEGF regulates PI3-K and/or and or MAPK activation in NSC34 cells 
12654515VEGFVEGF4.3VEGF induced concentration- and time-dependent increases in PI3-K and MAPK activities 
12654515VEGFVEGF-associated3.8and Fig 4 suggesting that these pathways may potentially mediate VEGF-associated motor neuron-like cell protection 3.4 
12654515VEGFVEGF-mediated3.8VEGF-mediated PI3-K activity not MAPK activity promotes mouse NSC34 motor neuron-like 
12654515VEGFVEGF-induced3.8respective contributions of the PI3-K and MAPK signaling pathways to VEGF-induced cell survival the PI3-K inhibitors LY294002 at 50 _amp_#x3bc M 
12654515VEGFVEGF4.3blockers reduced NSC34 cell viability even in the presence of VEGF ( Fig 5A while PD98059 did not modify cell survival 
12654515VEGFVEGF4.3PI3-K P85 promoted cell death even in the presence of VEGF while transfection with dominant negative MEK1 was void of any 
12654515VEGFVEGF4.3Activation of Akt by VEGF contributes to the protection from mutant SOD1-mediated motor neuron-like cell 
12654515VEGFVEGF4.3We therefore initially examined whether VEGF treatment of NSC34 cells was associated with Akt phosphorylation 
12654515VEGFVEGF4.3Indeed cells exposed to VEGF displayed concentration- and time-dependent Akt activation ( Fig 5D and 
12654515VEGFVEGF4.3resulted in a significant reduction in the protective effect by VEGF on survival of NSC34 cells infected with mutant G93A-SOD1 ( 
12654515VEGFVEGF4.3Taken together the data indicate that activation of Akt by VEGF contributes to the protection from NSC34 motor neuron-like cell death 
12654515VEGFVEGF4.3In this study we show that VEGF administration significantly protects from the decreased cell viability induced by 
12654515VEGFVEGF4.3We further demonstrate that the protective effects of VEGF are critically dependent on the activation of the PI3-K-Akt pathway 
12654515VEGFVEGF4.3lines of evidence prompted us to examine the effects of VEGF on mutant SOD1-mediated motor neuron-like cell death (i) i VEGF 
12654515VEGFVEGF4.3VEGF on mutant SOD1-mediated motor neuron-like cell death (i) i VEGF acts as a neurotrophic factor preventing hypoxia (ischemia)-mediated ischemia -mediated 
12654515VEGFVEGF4.3(iii) iii disruption of the hypoxic response elements in the VEGF promoter region of transgenic mice elicits a pattern of motor 
12654515VEGFVEGF4.3Thus one of the beneficial effects of VEGF on cell survival could theoretically be ascribed to a protective 
12654515VEGFVEGF4.3Our findings confirm such an hypothesis whereby VEGF is effective in preventing mutant SOD1-induced mouse NSC34 motor neuron-like 
12654515VEGFVEGF4.3VEGF was initially identified as an angiogenic factor that stimulates endothelial 
12654515VEGFVEGF4.3More recently VEGF was shown to induce neuroprotective functions both in vitro and 
12654515VEGFVEGF4.3For example VEGF rescues HN33 and hippocampal neuronal cells from the apoptosis induced 
12654515VEGFVEGF4.3Furthermore VEGF exerts direct neurotrophic effects on axonal outgrowth and neuronal survival 
12654515VEGFVEGF4.3Our current findings indicate that VEGF promotes motor neuron-like cell survival in the presence of mutant 
12654515VEGFVEGF4.3of mutant SOD1 thereby supporting the notion that deficits in VEGF protein induction or release may contribute to motor neuron degeneration 
12654515VEGFVEGF4.3These results also suggest that VEGF may have beneficial therapeutic effects in the prevention of motor 
12654515VEGFVEGF4.3It is well established that VEGF can activate both PI3-K and MAPK (MEK/ERK) MEK ERK pathways 
12654515VEGFVEGF4.3MAPK (MEK/ERK) MEK ERK pathways yet the protective effect of VEGF on motor neuron-like cell survival upon the expression of mutant 
12654515VEGFVEGF4.3PI3-K and MAPK pathways participate in neuronal cell protection by VEGF against glutamate excitotoxicity in primary rat hippocampal neuronal cultures 
12654515VEGFVEGF4.3possible that the PI3-K/Akt PI3-K Akt signaling module recruited by VEGF in our experiments is associated with survival and the activation 
12654515VEGFVEGF4.3expression of dominant negative Akt blocked the protective function of VEGF while the expression of constitutively active Akt partially prevented mutant 
12654515VEGFVEGF4.3SOD1-mediated motor neuron-like cell death even in the absence of VEGF ( Fig 5F 
12654515VEGFVEGF4.3It is unclear what apoptosis-related targets are specifically repressed by VEGF in the mutant SOD1-infected NSC34 motor neuron-like system 
12654515VEGFVEGF4.3However several lines of evidence suggest that the VEGF/Akt VEGF Akt pathway is particularly important to neuronal survival 
12654515VEGFVEGF4.3exposed to a pre-conditioning hypoxic stimulus up-regulated the expression of VEGF and Akt and the activity of the latter was critical 
12654515VEGFVEGF4.3Taken together these results suggest that hypoxia modulation of VEGF expression (activity) activity is essential to motor neuron survival 
12654515VEGFVEGF4.3that the activation of PI3-K/Akt PI3-K Akt signaling pathways by VEGF can promote motor neuron-like cell survival in the presence of 
12654515VEGFVEGF4.3transient event ( Fig 4 the long-lasting protective function of VEGF on mutant SOD1-mediated motor neuron-like cell death may be due 
12654515VEGFVEGF4.3In summary we have shown that VEGF can protect from mutant SOD1- and oxidative stress-mediated motor neuron-like 
12654515VEGFVEGF4.3activation is the primary contributor to the neuroprotective function of VEGF in mouse NSC34 motor neuron-like cells 
12654515VEGFVEGF4.3VEGF reduced hydrogen peroxide- TNF-_amp_#x3b1;- and mutant SOD1-mediated NSC34 motor neuron-like 
12654515VEGFVEGF4.3(A) A VEGF reduced hydrogen peroxide-mediated NSC34 motor neuron-like cell death 
12654515VEGFVEGF4.3NSC34 cells were pretreated with 100 ng/ml ng ml of VEGF or vehicle control for 30 min and then exposed to 
12654515VEGFVEGF4.3VEGF activated MAPK activity in mouse NSC34 motor neuron-like cells 
12654515VEGFVEGF4.3with different doses (25_amp_#x2013;200 25_amp_#x2013 200 ng/ml) ng ml of VEGF and then assayed for ERK1/2 ERK1 2 phosphorylation 
12654515VEGFVEGF4.3NSC34 cells were treated with 100 ng/ml ng ml of VEGF for different lengths of time (30_amp_#x2013;180 30_amp_#x2013 180 min and 
12654515VEGFVEGF4.3VEGF activated PI3-K activity in mouse NSC34 motor neuron-like cells 
12654515VEGFVEGF4.3(A) A NSC34 cells were treated with different doses of VEGF (25_amp_#x2013;200 25_amp_#x2013 200 ng/ml) ng ml and then assayed for 
12654515VEGFVEGF4.3NSC34 cells were treated with 100 ng/ml ng ml of VEGF for different lengths of time (30_amp_#x2013;180 30_amp_#x2013 180 min and 
12654515VEGFVEGF4.3Activation of PI3-K/Akt PI3-K Akt pathways by VEGF contributed to the protection from mutant G93A-SOD1-mediated NSC34 motor neuron-like 
12654515VEGFVEGF4.3NSC34 cells were treated with 100 ng/ml ng ml of VEGF for different lengths of time (30_amp_#x2013;180 30_amp_#x2013 180 min and 
12654515VEGFVEGF4.3while dominant negative Akt partially abolished the protective function of VEGF on NSC34 motor neuron survival upon expression of mutant G93A-SOD1 
14660707VEGFVEGF2.8on the observation that impaired vascular endothelial growth factor (VEGF) VEGF synthesis due to hypoxia selectively damages MNs ( Oosthuyse et 
16026864VEGFVEGF2.2that eliminates the ability of vascular endothelial-cell growth factor (VEGF) VEGF to respond to tissue hypoxia 54 
16026864VEGFVEGF2.2enhanced motoneuron degeneration 55 whereas treatment of SOD-transgenic mice with VEGF delayed progression of symptoms and prolonged survival 56 and 57 
16026864VEGFVEGF2.2Although direct neurotrophic effects of VEGF might contribute to these phenomena motoneurons seem selectively vulnerable to 
12654515vascular endothelial growth factorvascular endothelial growth factor1.0vascular endothelial growth factor vegf is neurotrophic and also protects from hypoxia induced neuronal injury.  
12654515vascular endothelial growth factorvascular endothelial growth factor1.0recently vascular endothelial growth factor vegf has been demonstrated to have neurotrophic effects by promoting neuronal cell survival in vitro and in vivo [ 23 26 43 and 45 ].  
12654515vascular permeability factorvascular permeability factor1.0vegf also known as vascular permeability factor is a dimeric glycoprotein that binds to endothelial cell specific receptors fms like tyrosine kinase flt 1 and fetal liver kinase flk 1 [ 16 and 36 ].  
14660707vascular endothelial growth factorvascular endothelial growth factor1.0this is based on the observation that impaired vascular endothelial growth factor vegf synthesis due to hypoxia selectively damages mns oosthuyse et al 2001 ; lambrechts et al 2003 .  
17192933vascular endothelial growth factorvascular endothelial growth factor1.0mt spinal cord organotypic slices secreted higher levels of nitric oxide interleukin il 1beta il 6 and il 12p70 and lower levels of vascular endothelial growth factor.  
17192933vascular endothelial growth factorvascular endothelial growth factor1.0the toxicity of mt spinal cord organotypic cultures was reduced and axonal lengths were restored to near normal by coculturing in the presence of reactive oxygen species scavenger vascular endothelial growth factor and neutralizing antibodies to il 1beta il 6 and il 12.