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10.1189/jlb.3A1014-480R http://scihub22266oqcxt.onion/10.1189/jlb.3A1014-480R C4600063!4600063 !26216936     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26216936 &cmd=llinks): Failed to open stream: HTTP request failed! 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Phospholipid scramblase 1 is required for ?2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation |pdf=|usr=}}{{26216936 }} gab.com Text Phospholipid scramblase 1 is required for 2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation JO: J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=26216936 #FOAvip Multiple pathologic conditions, including hemorrhage, tumor angiogenesis, and ischemia-reperfusion events, will result in hypoxia and subsequent reperfusion. Previous studies have analyzed the lipid changes within whole tissues and indicated that ischemia-reperfusion altered tissue and cellular phospholipids. Using an in vitro cell culture model of hypoxia and reoxygenation, we examined the endothelial lipid changes. We hypothesized that phospholipid scramblase 1, a protein that regulates bilayer asymmetry, is involved in altering the phospholipids of endothelial cells during hypoxia, a component of ischemia, leading to ?2-glycoprotein I and IgM binding and subsequent lipid-mediated, inflammatory responses. We have completed the first comprehensive study of steady-state phospholipid scramblase 1 mRNA levels, protein expression, and activity under conditions of hypoxia and reoxygenation. Phospholipid scramblase 1 regulates phosphatidylserine exposure in response to oxygen stress, leading to ?2-glycoprotein I and IgM binding and lipid-mediated, inflammatory responses. Twit Text FOAVip Phospholipid scramblase 1 is required for 2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation ????J Leukoc Biol http://www.kidney.de/pget.php?&tw=1&pmid=26216936 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26216936 #FOAvip English Wikipedia <ref>{{Cite pmid|26216936 }}</ref> Phospholipid scramblase 1 is required for ?2-glycoprotein I binding in hypoxia and reoxygenation-induced endothelial inflammation #MMPMID26216936 Slone EA ; Pope MR ; Fleming SD J Leukoc Biol 2015[Nov]; 98 (5 ): 791-804 PMID26216936 show ga Multiple pathologic conditions, including hemorrhage, tumor angiogenesis, and ischemia-reperfusion events, will result in hypoxia and subsequent reperfusion. Previous studies have analyzed the lipid changes within whole tissues and indicated that ischemia-reperfusion altered tissue and cellular phospholipids. Using an in vitro cell culture model of hypoxia and reoxygenation, we examined the endothelial lipid changes. We hypothesized that phospholipid scramblase 1, a protein that regulates bilayer asymmetry, is involved in altering the phospholipids of endothelial cells during hypoxia, a component of ischemia, leading to ?2-glycoprotein I and IgM binding and subsequent lipid-mediated, inflammatory responses. We have completed the first comprehensive study of steady-state phospholipid scramblase 1 mRNA levels, protein expression, and activity under conditions of hypoxia and reoxygenation. Phospholipid scramblase 1 regulates phosphatidylserine exposure in response to oxygen stress, leading to ?2-glycoprotein I and IgM binding and lipid-mediated, inflammatory responses. |Animals [MESH] |Cell Hypoxia [MESH] |Cell Line [MESH] |Endothelium, Vascular/*metabolism/pathology [MESH] |Immunoglobulin M/genetics/metabolism [MESH] |Inflammation/genetics/metabolism/pathology [MESH] |Mice [MESH] |Phospholipid Transfer Proteins/genetics/*metabolism [MESH] |Reperfusion Injury/genetics/*metabolism/pathology [MESH] |Vasculitis/genetics/*metabolism/pathology [MESH]Phospholipid scramblase 1 is required for ?2-glycoprotein I binding in(epmc).pdf DeepDyve Pubget Overpricing