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10.1016/j.ajpath.2014.08.015 http://scihub22266oqcxt.onion/10.1016/j.ajpath.2014.08.015 C4258496!4258496 !25307345     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25307345 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Pathol 2014 ; 184 (12 ): 3405-14 Nephropedia Template TP {{tp|p=25307345 |t=2014. The neurotensin-HIF-1?-VEGF? axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis |pdf=|usr=}}{{25307345 }} gab.com Text The neurotensin-HIF-1 -VEGF axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis JO: Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25307345 #FOAvip The expression of neurotensin (NT) and its receptor (NTR1) is up-regulated in experimental colitis and inflammatory bowel disease; NT/NTR1 interactions regulate gut inflammation. During active inflammation, metabolic shifts toward hypoxia lead to the activation of hypoxia-inducible factor (HIF)-1, which enhances vascular endothelial growth factor (VEGF) expression, promoting angiogenesis. We hypothesized that NT/NTR1 signaling regulates intestinal manifestations of hypoxia and angiogenesis by promoting HIF-1 transcriptional activity and VEGF? expression in experimental colitis. We studied NTR1 signaling in colitis-associated angiogenesis using 2,4,6-trinitrobenzenesulfonic acid-treated wild-type and NTR1-knockout mice. The effects of NT on HIF-1? and VEGF? were assessed on human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1) and human intestinal microvascular-endothelial cells. NTR1-knockout mice had reduced microvascular density and mucosal integrity score compared with wild-type mice after 2,4,6-trinitrobenzenesulfonic acid treatment. VEGF? mRNA levels were increased in NCM460-NTR1 cells treated with 10(-7) mol/L NT, at 1 and 6 hours post-treatment. NT exposure in NCM460-NTR1 cells caused stabilization, nuclear translocation, and transcriptional activity of HIF-1? in a diacylglycerol kinase-dependent manner. NT did not stimulate tube formation in isolated human intestinal macrovascular endothelial cells but did so in human intestinal macrovascular endothelial cells cocultured with NCM460-NTR1 cells. Our results demonstrate the importance of an NTR1-HIF-1?-VEGF? axis in intestinal angiogenic responses and in the pathophysiology of colitis and inflammatory bowel disease. Twit Text FOAVip The neurotensin-HIF-1 -VEGF axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis ????Am J Pathol http://www.kidney.de/pget.php?&tw=1&pmid=25307345 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25307345 #FOAvip English Wikipedia <ref>{{Cite pmid|25307345 }}</ref> The neurotensin-HIF-1?-VEGF? axis orchestrates hypoxia, colonic inflammation, and intestinal angiogenesis #MMPMID25307345 Bakirtzi K ; West G ; Fiocchi C ; Law IK ; Iliopoulos D ; Pothoulakis C Am J Pathol 2014[Dec]; 184 (12 ): 3405-14 PMID25307345 show ga The expression of neurotensin (NT) and its receptor (NTR1) is up-regulated in experimental colitis and inflammatory bowel disease; NT/NTR1 interactions regulate gut inflammation. During active inflammation, metabolic shifts toward hypoxia lead to the activation of hypoxia-inducible factor (HIF)-1, which enhances vascular endothelial growth factor (VEGF) expression, promoting angiogenesis. We hypothesized that NT/NTR1 signaling regulates intestinal manifestations of hypoxia and angiogenesis by promoting HIF-1 transcriptional activity and VEGF? expression in experimental colitis. We studied NTR1 signaling in colitis-associated angiogenesis using 2,4,6-trinitrobenzenesulfonic acid-treated wild-type and NTR1-knockout mice. The effects of NT on HIF-1? and VEGF? were assessed on human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1) and human intestinal microvascular-endothelial cells. NTR1-knockout mice had reduced microvascular density and mucosal integrity score compared with wild-type mice after 2,4,6-trinitrobenzenesulfonic acid treatment. VEGF? mRNA levels were increased in NCM460-NTR1 cells treated with 10(-7) mol/L NT, at 1 and 6 hours post-treatment. NT exposure in NCM460-NTR1 cells caused stabilization, nuclear translocation, and transcriptional activity of HIF-1? in a diacylglycerol kinase-dependent manner. NT did not stimulate tube formation in isolated human intestinal macrovascular endothelial cells but did so in human intestinal macrovascular endothelial cells cocultured with NCM460-NTR1 cells. Our results demonstrate the importance of an NTR1-HIF-1?-VEGF? axis in intestinal angiogenic responses and in the pathophysiology of colitis and inflammatory bowel disease. |Animals [MESH] |Colitis/pathology [MESH] |Colon/cytology/*pathology [MESH] |Disease Models, Animal [MESH] |Endothelial Cells/cytology [MESH] |Humans [MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/*metabolism [MESH] |Immunohistochemistry [MESH] |Inflammation/*metabolism [MESH] |Inflammatory Bowel Diseases/chemically induced/metabolism [MESH] |Intestinal Mucosa/*metabolism [MESH] |Intestines/blood supply [MESH] |Male [MESH] |Mice [MESH] |Microcirculation [MESH] |Neovascularization, Pathologic [MESH] |Receptors, Neurotensin/*metabolism [MESH] |Trinitrobenzenesulfonic Acid/chemistry [MESH] |Up-Regulation [MESH]The neurotensin-HIF-1?-VEGF? axis orchestrates hypoxia, colonic inflam(epmc).pdf DeepDyve Pubget Overpricing