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10.1371/journal.pone.0124362 http://scihub22266oqcxt.onion/10.1371/journal.pone.0124362 C4401453!4401453 !25884837     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25884837 &cmd=llinks): Failed to open stream: HTTP request failed! 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Pericytes contribute to the disruption of the cerebral endothelial barrier via increasing VEGF expression: implications for stroke |pdf=|usr=}}{{25884837 }} gab.com Text Pericytes contribute to the disruption of the cerebral endothelial barrier via increasing VEGF expression: implications for stroke JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25884837 #FOAvip Disruption of the blood-brain barrier (BBB) integrity occurring during the early onset of stroke is not only a consequence of, but also contributes to the further progression of stroke. Although it has been well documented that brain microvascular endothelial cells and astrocytes play a critical role in the maintenance of BBB integrity, pericytes, sandwiched between endothelial cells and astrocytes, remain poorly studied in the pathogenesis of stroke. Our findings demonstrated that treatment of human brain microvascular pericytes with sodium cyanide (NaCN) and glucose deprivation resulted in increased expression of vascular endothelial growth factor (VEGF) via the activation of tyrosine kinase Src, with downstream activation of mitogen activated protein kinase and PI3K/Akt pathways and subsequent translocation of NF-?B into the nucleus. Conditioned medium from NaCN-treated pericytes led to increased permeability of endothelial cells, and this effect was significantly inhibited by VEGF-neutralizing antibody. The in vivo relevance of these findings was further corroborated in the stroke model of mice wherein the mice, demonstrated disruption of the BBB integrity and concomitant increase in the expression of VEGF in the brain tissue as well as in the isolated microvessel. These findings thus suggest the role of pericyte-derived VEGF in modulating increased permeability of BBB during stroke. Understanding the regulation of VEGF expression could open new avenues for the development of potential therapeutic targets for stroke and other neurological disease. Twit Text FOAVip Pericytes contribute to the disruption of the cerebral endothelial barrier via increasing VEGF expression: implications for stroke ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25884837 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25884837 #FOAvip English Wikipedia <ref>{{Cite pmid|25884837 }}</ref> Pericytes contribute to the disruption of the cerebral endothelial barrier via increasing VEGF expression: implications for stroke #MMPMID25884837 Bai Y ; Zhu X ; Chao J ; Zhang Y ; Qian C ; Li P ; Liu D ; Han B ; Zhao L ; Zhang J ; Buch S ; Teng G ; Hu G ; Yao H PLoS One 2015[]; 10 (4 ): e0124362 PMID25884837 show ga Disruption of the blood-brain barrier (BBB) integrity occurring during the early onset of stroke is not only a consequence of, but also contributes to the further progression of stroke. Although it has been well documented that brain microvascular endothelial cells and astrocytes play a critical role in the maintenance of BBB integrity, pericytes, sandwiched between endothelial cells and astrocytes, remain poorly studied in the pathogenesis of stroke. Our findings demonstrated that treatment of human brain microvascular pericytes with sodium cyanide (NaCN) and glucose deprivation resulted in increased expression of vascular endothelial growth factor (VEGF) via the activation of tyrosine kinase Src, with downstream activation of mitogen activated protein kinase and PI3K/Akt pathways and subsequent translocation of NF-?B into the nucleus. Conditioned medium from NaCN-treated pericytes led to increased permeability of endothelial cells, and this effect was significantly inhibited by VEGF-neutralizing antibody. The in vivo relevance of these findings was further corroborated in the stroke model of mice wherein the mice, demonstrated disruption of the BBB integrity and concomitant increase in the expression of VEGF in the brain tissue as well as in the isolated microvessel. These findings thus suggest the role of pericyte-derived VEGF in modulating increased permeability of BBB during stroke. Understanding the regulation of VEGF expression could open new avenues for the development of potential therapeutic targets for stroke and other neurological disease. |*Blood-Brain Barrier [MESH] |Animals [MESH] |Cells, Cultured [MESH] |Endothelium, Vascular/*cytology/metabolism [MESH] |Genes, src [MESH] |Humans [MESH] |MAP Kinase Signaling System [MESH] |Male [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Pericytes/*cytology/metabolism [MESH] |Phosphatidylinositol 3-Kinases/metabolism [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH] |Sodium Cyanide/pharmacology [MESH] |Stroke/metabolism/*pathology [MESH] |Up-Regulation/drug effects [MESH]Pericytes contribute to the disruption of the cerebral endothelial bar(epmc).pdf DeepDyve Pubget Overpricing