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10.1172/JCI82788 http://scihub22266oqcxt.onion/10.1172/JCI82788 C4767341!4767341!26808499     free     free     free 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+Clin+Invest ä ; 126 (3): 837-53 Nephropedia Template TP {{tp|p=26808499|t=ä. PKC? inhibition normalizes the wound-healing capacity of diabetic human fibroblasts |pdf=|usr=}}{{26808499}} gab.com Text PKC inhibition normalizes the wound-healing capacity of diabetic human fibroblasts JO: J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26808499 #FOAvip Abnormal fibroblast function underlies poor wound healing in patients with diabetes; however, the mechanisms that impair wound healing are poorly defined. Here, we evaluated fibroblasts from individuals who had type 1 diabetes (T1D) for 50 years or more (Medalists, n = 26) and from age-matched controls (n = 7). Compared with those from controls, Medalist fibroblasts demonstrated a reduced migration response to insulin, lower VEGF expression, and less phosphorylated AKT (p-AKT), but not p-ERK, activation. Medalist fibroblasts were also functionally less effective at wound closure in nude mice. Activation of the ? isoform of protein kinase C (PKC?) was increased in postmortem fibroblasts from Medalists, fibroblasts from living T1D subjects, biopsies of active wounds of living T1D subjects, and granulation tissues from mice with streptozotocin-induced diabetes. Diabetes-induced PKCD mRNA expression was related to a 2-fold increase in the mRNA half-life. Pharmacologic inhibition and siRNA-mediated knockdown of PKC? or expression of a dominant-negative isoform restored insulin signaling of p-AKT and VEGF expression in vitro and improved wound healing in vivo. Additionally, increasing PKC? expression in control fibroblasts produced the same abnormalities as those seen in Medalist fibroblasts. Our results indicate that persistent PKC? elevation in fibroblasts from diabetic patients inhibits insulin signaling and function to impair wound healing and suggest PKC? inhibition as a potential therapy to improve wound healing in diabetic patients. Twit Text FOAVip PKC inhibition normalizes the wound-healing capacity of diabetic human fibroblasts ????J Clin Invest http://www.kidney.de/pget.php?&tw=1&pmid=26808499 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26808499 #FOAvip English Wikipedia <ref>{{Cite pmid|26808499}}</ref> PKC? inhibition normalizes the wound-healing capacity of diabetic human fibroblasts #MMPMID26808499 Khamaisi M; Katagiri S; Keenan H; Park K; Maeda Y; Li Q; Qi W; Thomou T; Eschuk D; Tellechea A; Veves A; Huang C; Orgill DP; Wagers A; King GL J Clin Invest ä[]; 126 (3): 837-53 PMID26808499show ga Abnormal fibroblast function underlies poor wound healing in patients with diabetes; however, the mechanisms that impair wound healing are poorly defined. Here, we evaluated fibroblasts from individuals who had type 1 diabetes (T1D) for 50 years or more (Medalists, n = 26) and from age-matched controls (n = 7). Compared with those from controls, Medalist fibroblasts demonstrated a reduced migration response to insulin, lower VEGF expression, and less phosphorylated AKT (p-AKT), but not p-ERK, activation. Medalist fibroblasts were also functionally less effective at wound closure in nude mice. Activation of the ? isoform of protein kinase C (PKC?) was increased in postmortem fibroblasts from Medalists, fibroblasts from living T1D subjects, biopsies of active wounds of living T1D subjects, and granulation tissues from mice with streptozotocin-induced diabetes. Diabetes-induced PKCD mRNA expression was related to a 2-fold increase in the mRNA half-life. Pharmacologic inhibition and siRNA-mediated knockdown of PKC? or expression of a dominant-negative isoform restored insulin signaling of p-AKT and VEGF expression in vitro and improved wound healing in vivo. Additionally, increasing PKC? expression in control fibroblasts produced the same abnormalities as those seen in Medalist fibroblasts. Our results indicate that persistent PKC? elevation in fibroblasts from diabetic patients inhibits insulin signaling and function to impair wound healing and suggest PKC? inhibition as a potential therapy to improve wound healing in diabetic patients. äPKC? inhibition normalizes the wound-healing capacity of diabetic huma(epmc).pdf DeepDyve Pubget Overpricing