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10.1161/ATVBAHA.114.304705 http://scihub22266oqcxt.onion/10.1161/ATVBAHA.114.304705 C5873604!5873604 !25395617     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25395617 &cmd=llinks): Failed to open stream: HTTP request failed! 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Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2 dephosphorylation |pdf=|usr=}}{{25395617 }} gab.com Text Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2 dephosphorylation JO: Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25395617 #FOAvip OBJECTIVE: Impaired wound healing is a major complication of diabetes mellitus. The mechanisms that govern wound healing, however, are complex and incompletely understood. In the present study, we determined the inhibitory role of protein tyrosine phosphatase 1B (PTP1B) in the process of diabetic wound healing. APPROACH AND RESULTS: First, by comparing the wound healing process in PTP1B knockout (PTP1B(-/-)) mice, ob/ob mice and their wild-type littermates in the presence or absence of streptozotocin treatment, we showed that the inhibition of mouse wound healing in streptozotocin-induced diabetic conditions is because of the upregulation and activation of PTP1B. Second, the impaired wound healing in ob/ob mice and streptozotocin-treated wild-type mice was rescued by a PTP1B inhibitor. Third, PTP1B, which is upregulated under hyperglycemic condition, inhibited the tube formation, proliferation, and migration of human microvascular endothelial cells induced by vascular endothelial growth factor, whereas this inhibition was largely abolished by the PTP1B inhibitor. Finally, mechanism study further indicated that PTP1B likely suppressed the proliferation, migration, and tube formation of vascular endothelial cells through dephosphorylation of vascular endothelial growth factor receptor 2. CONCLUSIONS: Our study demonstrated that PTP1B negatively modulated the diabetic wound healing process by dephosphorylating the endothelial cell vascular endothelial growth factor receptor 2 and that the specific inhibitor of PTP1B might serve as a potential novel therapeutic tool for diabetic wound healing. Twit Text FOAVip Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2 dephosphorylation ????Arterioscler Thromb Vasc Biol http://www.kidney.de/pget.php?&tw=1&pmid=25395617 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25395617 #FOAvip English Wikipedia <ref>{{Cite pmid|25395617 }}</ref> Protein tyrosine phosphatase 1B impairs diabetic wound healing through vascular endothelial growth factor receptor 2 dephosphorylation #MMPMID25395617 Zhang J ; Li L ; Li J ; Liu Y ; Zhang CY ; Zhang Y ; Zen K Arterioscler Thromb Vasc Biol 2015[Jan]; 35 (1 ): 163-74 PMID25395617 show ga OBJECTIVE: Impaired wound healing is a major complication of diabetes mellitus. The mechanisms that govern wound healing, however, are complex and incompletely understood. In the present study, we determined the inhibitory role of protein tyrosine phosphatase 1B (PTP1B) in the process of diabetic wound healing. APPROACH AND RESULTS: First, by comparing the wound healing process in PTP1B knockout (PTP1B(-/-)) mice, ob/ob mice and their wild-type littermates in the presence or absence of streptozotocin treatment, we showed that the inhibition of mouse wound healing in streptozotocin-induced diabetic conditions is because of the upregulation and activation of PTP1B. Second, the impaired wound healing in ob/ob mice and streptozotocin-treated wild-type mice was rescued by a PTP1B inhibitor. Third, PTP1B, which is upregulated under hyperglycemic condition, inhibited the tube formation, proliferation, and migration of human microvascular endothelial cells induced by vascular endothelial growth factor, whereas this inhibition was largely abolished by the PTP1B inhibitor. Finally, mechanism study further indicated that PTP1B likely suppressed the proliferation, migration, and tube formation of vascular endothelial cells through dephosphorylation of vascular endothelial growth factor receptor 2. CONCLUSIONS: Our study demonstrated that PTP1B negatively modulated the diabetic wound healing process by dephosphorylating the endothelial cell vascular endothelial growth factor receptor 2 and that the specific inhibitor of PTP1B might serve as a potential novel therapeutic tool for diabetic wound healing. |*Wound Healing/drug effects [MESH] |Animals [MESH] |Cell Line [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Diabetes Mellitus, Experimental/drug therapy/*enzymology/genetics/pathology/physiopathology [MESH] |Diabetic Angiopathies/drug therapy/*enzymology/genetics/pathology/physiopathology [MESH] |Endothelial Cells/drug effects/*enzymology [MESH] |Enzyme Activation [MESH] |Enzyme Inhibitors/pharmacology [MESH] |Humans [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Neovascularization, Physiologic [MESH] |Phosphorylation [MESH] |Protein Tyrosine Phosphatase, Non-Receptor Type 1/antagonists & inhibitors/deficiency/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Skin Ulcer/drug therapy/*enzymology/genetics/pathology/physiopathology [MESH] |Time Factors [MESH] |Transfection [MESH] |Up-Regulation [MESH]Protein tyrosine phosphatase 1B impairs diabetic wound healing through(epmc).pdf DeepDyve Pubget Overpricing