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10.1093/cvr/cvu116 http://scihub22266oqcxt.onion/10.1093/cvr/cvu116 24788415!4133591!24788415     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 247.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cardiovasc+Res 2014 ; 103 (1): 131-9 Nephropedia Template TP {{tp|p=24788415|t=2014. Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory responsedagger |pdf=|usr=}}{{24788415}} gab.com Text Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory responsedagger JO: Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=24788415 #FOAvip AIMS: Hypoxia induces vascular inflammation by a mechanism not fully understood. Emerging evidence implicates O-GlcNAc transferase (OGT) in inflammation. This study explored the role of OGT in hypoxia-induced vascular endothelial inflammatory response. METHODS AND RESULTS: Hypoxia was either induced (1% O2 chamber) or mimicked by exposure to hypoxia-mimetic agents in cultured endothelial cells. Hypoxia increased hypoxia-inducible factor (HIF-1alpha) and inflammatory response (gene and protein expression of interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and E-selectin) but, surprisingly, reduced OGT protein (not mRNA) levels. Hypoxia-mimetic CoCl2 failed to reduce OGT when proteasome inhibitors were present, suggesting proteasome involvement. Indeed, CoCl2 enhanced 26S proteasome functionality evidenced by diminished reporter (Ub(G76V)-GFP) proteins in proteasome reporter cells, likely due to increased chymotrypsin-like activities. Mechanistically, beta-TrCP1 mediated OGT degradation, since siRNA ablation of this E3 ubiquitin ligase stabilized OGT. Administration of the oxidative stress inhibitors reversed both proteasome activation and OGT degradation. Furthermore, up-regulation of OGT by stabilization, overexpression, or activation mitigated CoCl2-elicited inflammatory response. These observations were recapitulated in a mouse (C57BL/6J) model mimicking hypoxia, in which lung tissues presented higher levels of HIF-1alpha, proteasome activity, and inflammatory response, but lower levels of OGT (n = 5/group, hypoxia vs. normoxia, P < 0.05). However, administration of an activator of OGT (glucosamine: 1 mg/g/day, vehicle: saline, ip, 5 days) abolished the up-regulation of proteasome activity and inflammatory response (n = 5/group, the treated vs. untreated hypoxia groups, P < 0.05). CONCLUSIONS: 26S proteasome-mediated OGT reduction contributed to hypoxia-induced vascular endothelial inflammatory response. Modulation of OGT may represent a new approach to treat diseases characterized by hypoxic inflammation. Twit Text FOAVip Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory responsedagger ????Cardiovasc Res http://www.kidney.de/pget.php?&tw=1&pmid=24788415 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24788415 #FOAvip English Wikipedia <ref>{{Cite pmid|24788415}}</ref> Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induced vascular endothelial inflammatory responsedagger #MMPMID24788415 Liu H; Wang Z; Yu S; Xu J Cardiovasc Res 2014[Jul]; 103 (1): 131-9 PMID24788415show ga AIMS: Hypoxia induces vascular inflammation by a mechanism not fully understood. Emerging evidence implicates O-GlcNAc transferase (OGT) in inflammation. This study explored the role of OGT in hypoxia-induced vascular endothelial inflammatory response. METHODS AND RESULTS: Hypoxia was either induced (1% O2 chamber) or mimicked by exposure to hypoxia-mimetic agents in cultured endothelial cells. Hypoxia increased hypoxia-inducible factor (HIF-1alpha) and inflammatory response (gene and protein expression of interleukin (IL)-6, IL-8, monocyte chemoattractant protein-1, and E-selectin) but, surprisingly, reduced OGT protein (not mRNA) levels. Hypoxia-mimetic CoCl2 failed to reduce OGT when proteasome inhibitors were present, suggesting proteasome involvement. Indeed, CoCl2 enhanced 26S proteasome functionality evidenced by diminished reporter (Ub(G76V)-GFP) proteins in proteasome reporter cells, likely due to increased chymotrypsin-like activities. Mechanistically, beta-TrCP1 mediated OGT degradation, since siRNA ablation of this E3 ubiquitin ligase stabilized OGT. Administration of the oxidative stress inhibitors reversed both proteasome activation and OGT degradation. Furthermore, up-regulation of OGT by stabilization, overexpression, or activation mitigated CoCl2-elicited inflammatory response. These observations were recapitulated in a mouse (C57BL/6J) model mimicking hypoxia, in which lung tissues presented higher levels of HIF-1alpha, proteasome activity, and inflammatory response, but lower levels of OGT (n = 5/group, hypoxia vs. normoxia, P < 0.05). However, administration of an activator of OGT (glucosamine: 1 mg/g/day, vehicle: saline, ip, 5 days) abolished the up-regulation of proteasome activity and inflammatory response (n = 5/group, the treated vs. untreated hypoxia groups, P < 0.05). CONCLUSIONS: 26S proteasome-mediated OGT reduction contributed to hypoxia-induced vascular endothelial inflammatory response. Modulation of OGT may represent a new approach to treat diseases characterized by hypoxic inflammation. |Animals[MESH] |Cobalt/toxicity[MESH] |Endothelium, Vascular/drug effects/*metabolism/pathology[MESH] |Enzyme Stability[MESH] |Human Umbilical Vein Endothelial Cells[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/metabolism[MESH] |Hypoxia/complications/*metabolism/pathology[MESH] |Inflammation/etiology/*metabolism/pathology[MESH] |Male[MESH] |Mice[MESH] |Mice, Inbred C57BL[MESH] |N-Acetylglucosaminyltransferases/*metabolism[MESH] |Proteasome Endopeptidase Complex/metabolism[MESH] |Proteolysis[MESH] |Reactive Nitrogen Species/metabolism[MESH] |Reactive Oxygen Species/metabolism[MESH] |Ubiquitin-Protein Ligases/metabolism[MESH]Proteasomal degradation of O-GlcNAc transferase elevates hypoxia-induc(epmc).pdf DeepDyve Pubget Overpricing