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10.1016/j.neulet.2015.10.051 http://scihub22266oqcxt.onion/10.1016/j.neulet.2015.10.051 26518240!?!26518240 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26518240&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Neurosci+Lett 2016 ; 610 (?): 54-9 Nephropedia Template TP {{tp|p=26518240|t=2016. VEGF-mediated NF-kappaB activation protects PC12 cells from damage induced by hypoxia |pdf=|usr=}}{{26518240}} gab.com Text VEGF-mediated NF-kappaB activation protects PC12 cells from damage induced by hypoxia JO: Neurosci Lett http://www.kidney.de/pget.php?&tw=1&pmid=26518240 #FOAvip Neuronal apoptosis is a contributing cause of disability and death in cerebral ischemia. Nuclear factor-kappaB (NF-kappaB) may become a potential therapeutic target for hypoxic/ischemic neuron damage because NF-kappaB is inactivated after hypoxia exposure. Vascular endothelial growth factor (VEGF) has been found to improve neurological function recovery in cerebral ischemic injury although the exact molecular mechanisms that underlie the neuroprotective function of VEGF remain largely unknown. Here we defined the mechanism by which VEGF antagonized neuron-like PC12 cells apoptosis induced by hypoxia mimetic agent cobalt chloride (CoCl2) is through restoration of NF-kappaB activity. Depletion of VEGF with small interfering RNA (siRNA) in PC12 cells conferred CoCl2-induced cytotoxicity which was mitigated by VEGF administration. Treatment of PC12 cells with VEGF attenuated the CoCl2-induced cytotoxicity in both dose- and time-dependent manner. Mechanistically, VEGF increased IkappaBalpha phosphorylation and ubiquitination, promoted P65 nuclear translocation as well as upregulated XIAP and CCND1 expression. Meanwhile, VEGF administration reversed the dysregulation of IkappaBalpha phosphorylation and ubiquitination, P65 nuclear translocation as well as XIAP and CCND1 expression induced by CoCl2. Notably, the VEGF-dependent cytoprotection was abolished by pretreatment with BAY 11-7085, a specific inhibitor of NF-kappaB. Our data suggest that VEGF/NF-kappaB signalling pathway represents an adaptive mechanism that protects neural cells against hypoxic damage. Twit Text FOAVip VEGF-mediated NF-kappaB activation protects PC12 cells from damage induced by hypoxia ????Neurosci Lett http://www.kidney.de/pget.php?&tw=1&pmid=26518240 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26518240 #FOAvip English Wikipedia <ref>{{Cite pmid|26518240}}</ref> VEGF-mediated NF-kappaB activation protects PC12 cells from damage induced by hypoxia #MMPMID26518240 Mo SJ; Hong J; Chen X; Han F; Ni Y; Zheng Y; Liu JQ; Xu L; Li Q; Yang XH; Sun RH; Yin XY Neurosci Lett 2016[Jan]; 610 (?): 54-9 PMID26518240show ga Neuronal apoptosis is a contributing cause of disability and death in cerebral ischemia. Nuclear factor-kappaB (NF-kappaB) may become a potential therapeutic target for hypoxic/ischemic neuron damage because NF-kappaB is inactivated after hypoxia exposure. Vascular endothelial growth factor (VEGF) has been found to improve neurological function recovery in cerebral ischemic injury although the exact molecular mechanisms that underlie the neuroprotective function of VEGF remain largely unknown. Here we defined the mechanism by which VEGF antagonized neuron-like PC12 cells apoptosis induced by hypoxia mimetic agent cobalt chloride (CoCl2) is through restoration of NF-kappaB activity. Depletion of VEGF with small interfering RNA (siRNA) in PC12 cells conferred CoCl2-induced cytotoxicity which was mitigated by VEGF administration. Treatment of PC12 cells with VEGF attenuated the CoCl2-induced cytotoxicity in both dose- and time-dependent manner. Mechanistically, VEGF increased IkappaBalpha phosphorylation and ubiquitination, promoted P65 nuclear translocation as well as upregulated XIAP and CCND1 expression. Meanwhile, VEGF administration reversed the dysregulation of IkappaBalpha phosphorylation and ubiquitination, P65 nuclear translocation as well as XIAP and CCND1 expression induced by CoCl2. Notably, the VEGF-dependent cytoprotection was abolished by pretreatment with BAY 11-7085, a specific inhibitor of NF-kappaB. Our data suggest that VEGF/NF-kappaB signalling pathway represents an adaptive mechanism that protects neural cells against hypoxic damage. |Animals[MESH] |Cell Hypoxia[MESH] |Cobalt/pharmacology[MESH] |NF-kappa B/*metabolism[MESH] |PC12 Cells[MESH] |Rats[MESH] |Signal Transduction[MESH]VEGF-mediated NF-kappaB activation protects PC12 cells from damage ind(epmc).pdf DeepDyve Pubget Overpricing