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10.4049/jimmunol.1500936 http://scihub22266oqcxt.onion/10.4049/jimmunol.1500936 C4560490!4560490!26276873     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       J+Immunol 2015 ; 195 (6): 2852-60 Nephropedia Template TP {{tp|p=26276873|t=2015. Lipoxin A4 Attenuates Constitutive and TGF-?1?Dependent Profibrotic Activity in Human Lung Myofibroblasts |pdf=|usr=}}{{26276873}} gab.com Text Lipoxin A4 Attenuates Constitutive and TGF- 1 Dependent Profibrotic Activity in Human Lung Myofibroblasts JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26276873 #FOAvip Idiopathic pulmonary fibrosis (IPF) is a common, progressive, and invariably lethal interstitial lung disease with no effective therapy. The key cell driving the development of fibrosis is the myofibroblast. Lipoxin A4 (LXA4) is an anti-inflammatory lipid, important in the resolution of inflammation, and it has potential antifibrotic activity. However, the effects of LXA4 on primary human lung myofibroblasts (HLMFs) have not previously been investigated. Therefore, the aim of this study was to examine the effects of LXA4 on TGF-?1?dependent responses in IPF- and nonfibrotic control (NFC)?derived HLMFs. HLMFs were isolated from IPF and NFC patients and grown in vitro. The effects of LXA4 on HLMF proliferation, collagen secretion, ?-smooth muscle actin (?SMA) expression, and Smad2/3 activation were examined constitutively and following TGF-?1 stimulation. The LXA4 receptor (ALXR) was expressed in both NFC- and IPF-derived HLMFs. LXA4 (10?10 and 10?8 mol) reduced constitutive ?SMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3, indicating regression from a myofibroblast to fibroblast phenotype. LXA4 also significantly inhibited FBS-dependent proliferation and TGF-?1?dependent collagen secretion, ?SMA expression, and Smad2/3 nuclear translocation in IPF-derived HLMFs. LXA4 did not inhibit Smad2/3 phosphorylation. In summary, LXA4 attenuated profibrotic HLMF activity and promoted HLMF regression to a quiescent fibroblast phenotype. LXA4 or its stable analogs delivered by aerosol may offer a novel approach to the treatment of IPF. Twit Text FOAVip Lipoxin A4 Attenuates Constitutive and TGF- 1 Dependent Profibrotic Activity in Human Lung Myofibroblasts ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=26276873 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26276873 #FOAvip English Wikipedia <ref>{{Cite pmid|26276873}}</ref> Lipoxin A4 Attenuates Constitutive and TGF-?1?Dependent Profibrotic Activity in Human Lung Myofibroblasts #MMPMID26276873 Roach KM; Feghali-Bostwick CA; Amrani Y; Bradding P J Immunol 2015[Sep]; 195 (6): 2852-60 PMID26276873show ga Idiopathic pulmonary fibrosis (IPF) is a common, progressive, and invariably lethal interstitial lung disease with no effective therapy. The key cell driving the development of fibrosis is the myofibroblast. Lipoxin A4 (LXA4) is an anti-inflammatory lipid, important in the resolution of inflammation, and it has potential antifibrotic activity. However, the effects of LXA4 on primary human lung myofibroblasts (HLMFs) have not previously been investigated. Therefore, the aim of this study was to examine the effects of LXA4 on TGF-?1?dependent responses in IPF- and nonfibrotic control (NFC)?derived HLMFs. HLMFs were isolated from IPF and NFC patients and grown in vitro. The effects of LXA4 on HLMF proliferation, collagen secretion, ?-smooth muscle actin (?SMA) expression, and Smad2/3 activation were examined constitutively and following TGF-?1 stimulation. The LXA4 receptor (ALXR) was expressed in both NFC- and IPF-derived HLMFs. LXA4 (10?10 and 10?8 mol) reduced constitutive ?SMA expression, actin stress fiber formation, contraction, and nuclear Smad2/3, indicating regression from a myofibroblast to fibroblast phenotype. LXA4 also significantly inhibited FBS-dependent proliferation and TGF-?1?dependent collagen secretion, ?SMA expression, and Smad2/3 nuclear translocation in IPF-derived HLMFs. LXA4 did not inhibit Smad2/3 phosphorylation. In summary, LXA4 attenuated profibrotic HLMF activity and promoted HLMF regression to a quiescent fibroblast phenotype. LXA4 or its stable analogs delivered by aerosol may offer a novel approach to the treatment of IPF. äLipoxin A4 Attenuates Constitutive and TGF-?1?Dependent Profibrotic Ac(epmc).pdf DeepDyve Pubget Overpricing