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10.1242/jcs.163774 http://scihub22266oqcxt.onion/10.1242/jcs.163774 C4487014!4487014!25956888     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25956888&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 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Cell+Sci 2015 ; 128 (12): 2236-48 Nephropedia Template TP {{tp|p=25956888|t=2015. Autocrine VEGF maintains endothelial survival through regulation of metabolism and autophagy |pdf=|usr=}}{{25956888}} gab.com Text Autocrine VEGF maintains endothelial survival through regulation of metabolism and autophagy JO: J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=25956888 #FOAvip Autocrine VEGF is necessary for endothelial survival, although the cellular mechanisms supporting this function are unknown. Here, we show that ? even after full differentiation and maturation ? continuous expression of VEGF by endothelial cells is needed to sustain vascular integrity and cellular viability. Depletion of VEGF from the endothelium results in mitochondria fragmentation and suppression of glucose metabolism, leading to increased autophagy that contributes to cell death. Gene-expression profiling showed that endothelial VEGF contributes to the regulation of cell cycle and mitochondrial gene clusters, as well as several ? but not all ? targets of the transcription factor FOXO1. Indeed, VEGF-deficient endothelium in vitro and in vivo showed increased levels of FOXO1 protein in the nucleus and cytoplasm. Silencing of FOXO1 in VEGF-depleted cells reversed expression profiles of several of the gene clusters that were de-regulated in VEGF knockdown, and rescued both cell death and autophagy phenotypes. Our data suggest that endothelial VEGF maintains vascular homeostasis through regulation of FOXO1 levels, thereby ensuring physiological metabolism and endothelial cell survival. Twit Text FOAVip Autocrine VEGF maintains endothelial survival through regulation of metabolism and autophagy ????J Cell Sci http://www.kidney.de/pget.php?&tw=1&pmid=25956888 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25956888 #FOAvip English Wikipedia <ref>{{Cite pmid|25956888}}</ref> Autocrine VEGF maintains endothelial survival through regulation of metabolism and autophagy #MMPMID25956888 Domigan CK; Warren CM; Antanesian V; Happel K; Ziyad S; Lee S; Krall A; Duan L; Torres-Collado AX; Castellani LW; Elashoff D; Christofk HR; van der Bliek AM; Potente M; Iruela-Arispe ML J Cell Sci 2015[Jun]; 128 (12): 2236-48 PMID25956888show ga Autocrine VEGF is necessary for endothelial survival, although the cellular mechanisms supporting this function are unknown. Here, we show that ? even after full differentiation and maturation ? continuous expression of VEGF by endothelial cells is needed to sustain vascular integrity and cellular viability. Depletion of VEGF from the endothelium results in mitochondria fragmentation and suppression of glucose metabolism, leading to increased autophagy that contributes to cell death. Gene-expression profiling showed that endothelial VEGF contributes to the regulation of cell cycle and mitochondrial gene clusters, as well as several ? but not all ? targets of the transcription factor FOXO1. Indeed, VEGF-deficient endothelium in vitro and in vivo showed increased levels of FOXO1 protein in the nucleus and cytoplasm. Silencing of FOXO1 in VEGF-depleted cells reversed expression profiles of several of the gene clusters that were de-regulated in VEGF knockdown, and rescued both cell death and autophagy phenotypes. Our data suggest that endothelial VEGF maintains vascular homeostasis through regulation of FOXO1 levels, thereby ensuring physiological metabolism and endothelial cell survival. äAutocrine VEGF maintains endothelial survival through regulation of me(epmc).pdf DeepDyve Pubget Overpricing