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10.1038/cddis.2017.375 http://scihub22266oqcxt.onion/10.1038/cddis.2017.375 C5596563!5596563!28796258     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (8): e2976- Nephropedia Template TP {{tp|p=28796258|t=2017. Loss of PHD3 in myeloid cells dampens the inflammatory response and fibrosis after hind-limb ischemia |pdf=|usr=}}{{28796258}} gab.com Text Loss of PHD3 in myeloid cells dampens the inflammatory response and fibrosis after hind-limb ischemia JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28796258 #FOAvip Macrophages are essential for the inflammatory response after an ischemic insult and thereby influence tissue recovery. For the oxygen sensing prolyl-4-hydroxylase domain enzyme (PHD) 2 a clear impact on the macrophage-mediated arteriogenic response after hind-limb ischemia has been demonstrated previously, which involves fine tuning a M2-like macrophage population. To analyze the role of PHD3 in macrophages, we performed hind-limb ischemia (ligation and excision of the femoral artery) in myeloid-specific PHD3 knockout mice (PHD3?/?) and analyzed the inflammatory cell invasion, reperfusion recovery and fibrosis in the ischemic muscle post-surgery. In contrast to PHD2, reperfusion recovery and angiogenesis was unaltered in PHD3?/? compared to WT mice. Macrophages from PHD3?/? mice showed, however, a dampened inflammatory reaction in the affected skeletal muscle tissues compared to WT controls. This was associated with a decrease in fibrosis and an anti-inflammatory phenotype of the PHD3?/? macrophages, as well as decreased expression of Cyp2s1 and increased PGE2-secretion, which could be mimicked by PHD3?/? bone marrow-derived macrophages in serum starvation. Twit Text FOAVip Loss of PHD3 in myeloid cells dampens the inflammatory response and fibrosis after hind-limb ischemia ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28796258 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28796258 #FOAvip English Wikipedia <ref>{{Cite pmid|28796258}}</ref> Loss of PHD3 in myeloid cells dampens the inflammatory response and fibrosis after hind-limb ischemia #MMPMID28796258 Beneke A; Guentsch A; Hillemann A; Zieseniss A; Swain L; Katschinski DM Cell Death Dis 2017[Aug]; 8 (8): e2976- PMID28796258show ga Macrophages are essential for the inflammatory response after an ischemic insult and thereby influence tissue recovery. For the oxygen sensing prolyl-4-hydroxylase domain enzyme (PHD) 2 a clear impact on the macrophage-mediated arteriogenic response after hind-limb ischemia has been demonstrated previously, which involves fine tuning a M2-like macrophage population. To analyze the role of PHD3 in macrophages, we performed hind-limb ischemia (ligation and excision of the femoral artery) in myeloid-specific PHD3 knockout mice (PHD3?/?) and analyzed the inflammatory cell invasion, reperfusion recovery and fibrosis in the ischemic muscle post-surgery. In contrast to PHD2, reperfusion recovery and angiogenesis was unaltered in PHD3?/? compared to WT mice. Macrophages from PHD3?/? mice showed, however, a dampened inflammatory reaction in the affected skeletal muscle tissues compared to WT controls. This was associated with a decrease in fibrosis and an anti-inflammatory phenotype of the PHD3?/? macrophages, as well as decreased expression of Cyp2s1 and increased PGE2-secretion, which could be mimicked by PHD3?/? bone marrow-derived macrophages in serum starvation. äLoss of PHD3 in myeloid cells dampens the inflammatory response and fi(epmc).pdf DeepDyve Pubget Overpricing