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10.1111/jth.13072 http://scihub22266oqcxt.onion/10.1111/jth.13072 C4877623!4877623!26264622     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 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Thromb+Haemost 2015 ; 13 (10): 1928-40 Nephropedia Template TP {{tp|p=26264622|t=2015. A novel pathway of cellular activation mediated by antiphospholipid antibody-induced extracellular vesicles |pdf=|usr=}}{{26264622}} gab.com Text A novel pathway of cellular activation mediated by antiphospholipid antibody-induced extracellular vesicles JO: J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=26264622 #FOAvip Background: Elevated levels of endothelial cell (EC)-derived extracellular vesicles (EVs) circulate in patients with antiphospholipid antibodies (APLAs), and APLAs, particularly those against ?2-glycoprotein I (?2GPI), stimulate EV release from ECs. However, the effects of EC-derived EVs have not been characterized. Objective: To determine the mechanism by which EVs released from ECs by anti-?2GPI antibodies activate unstimulated ECs. Patients/methods: We used interleukin (IL)-1 receptor inhibitors, small interfering RNA (siRNA) against Toll-like receptors (TLRs) and microRNA (miRNA) profiling to assess the mechanism(s) by which EVs released from ECs exposed to anti-?2GPI antibodies activated unstimulated ECs. Results and conclusions: Anti-?2GPI antibodies caused formation of an EC inflammasome and the release of EVs that were enriched in mature IL-1?, had a distinct miRNA profile, and caused endothelial activation. However, activation was not inhibited by an IL-1? antibody, an IL-1 receptor antagonist, or IL-1 receptor siRNA. EC activation by EVs required IL-1 receptor-associated kinase 4 phosphorylation, and was inhibited by pretreatment of cells with TLR7 siRNA or RNase A, which degrades ssRNA. Profiling of miRNA in EVs released from ECs incubated with ?2GPI and either control IgG or anti-?2GPI antibodies revealed numerous differences in the content of specific miRNAs, including a significant decrease in mIR126. These observations demonstrate that, although anti-?2GPI-derived endothelial EVs contain IL-1?, they activate unstimulated ECs through a TLR7-dependent and ssRNA-dependent pathway. Alterations in miRNA content may contribute to the ability of EVs derived from ECs exposed to anti-?2GPI antibodies to activate unstimulated ECs in an autocrine or paracrine manner. Twit Text FOAVip A novel pathway of cellular activation mediated by antiphospholipid antibody-induced extracellular vesicles ????J Thromb Haemost http://www.kidney.de/pget.php?&tw=1&pmid=26264622 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26264622 #FOAvip English Wikipedia <ref>{{Cite pmid|26264622}}</ref> A novel pathway of cellular activation mediated by antiphospholipid antibody-induced extracellular vesicles #MMPMID26264622 WU M; BARNARD J; KUNDU S; MCCRAE KR J Thromb Haemost 2015[Oct]; 13 (10): 1928-40 PMID26264622show ga Background: Elevated levels of endothelial cell (EC)-derived extracellular vesicles (EVs) circulate in patients with antiphospholipid antibodies (APLAs), and APLAs, particularly those against ?2-glycoprotein I (?2GPI), stimulate EV release from ECs. However, the effects of EC-derived EVs have not been characterized. Objective: To determine the mechanism by which EVs released from ECs by anti-?2GPI antibodies activate unstimulated ECs. Patients/methods: We used interleukin (IL)-1 receptor inhibitors, small interfering RNA (siRNA) against Toll-like receptors (TLRs) and microRNA (miRNA) profiling to assess the mechanism(s) by which EVs released from ECs exposed to anti-?2GPI antibodies activated unstimulated ECs. Results and conclusions: Anti-?2GPI antibodies caused formation of an EC inflammasome and the release of EVs that were enriched in mature IL-1?, had a distinct miRNA profile, and caused endothelial activation. However, activation was not inhibited by an IL-1? antibody, an IL-1 receptor antagonist, or IL-1 receptor siRNA. EC activation by EVs required IL-1 receptor-associated kinase 4 phosphorylation, and was inhibited by pretreatment of cells with TLR7 siRNA or RNase A, which degrades ssRNA. Profiling of miRNA in EVs released from ECs incubated with ?2GPI and either control IgG or anti-?2GPI antibodies revealed numerous differences in the content of specific miRNAs, including a significant decrease in mIR126. These observations demonstrate that, although anti-?2GPI-derived endothelial EVs contain IL-1?, they activate unstimulated ECs through a TLR7-dependent and ssRNA-dependent pathway. Alterations in miRNA content may contribute to the ability of EVs derived from ECs exposed to anti-?2GPI antibodies to activate unstimulated ECs in an autocrine or paracrine manner. äA novel pathway of cellular activation mediated by antiphospholipid an(epmc).pdf DeepDyve Pubget Overpricing