caa a22 4500 445885777 CHVBK 20180317145559.0 cr unu---uuuuu 170323e20110801xx s 000 0 eng 10.1007/s00011-011-0326-5 doi (NATIONALLICENCE)springer-10.1007/s00011-011-0326-5 Lipopolysaccharide and platelet-activating factor stimulate expression of platelet-activating factor acetylhydrolase via distinct signaling pathways [Elektronische Daten] [Katherine Howard, Mohammed Abdel-al, Marcia Ditmyer, Nipa Patel] Objectives: This study was designed to investigate and characterize the ability of platelet-activating factor (PAF) to induce the expression of platelet-activating factor acetylhydrolase (PAF-AH). Methods: Ribonuclease protection assays and quantitative real-time PCR were used to investigate the ability of lipopolysaccharide (LPS) and PAF to regulate PAF-AH mRNA expression in human monocyte-macrophage 6 (MM6) cells. Pharmacological inhibitors of mitogen activated protein kinases (MAPK) and PAF receptor antagonists were used to investigate the mechanism of regulation of PAF-AH. Results: PAF-AH mRNA levels were increased upon exposure to LPS or PAF in a dose-dependent manner. LPS elicited a more potent and rapid increase in PAF-AH expression than the PAF-stimulated response. However, when administered concomitantly, PAF augmented the LPS-stimulated response. LPS-stimulated PAF-AH expression was susceptible to partial inhibition by a p38 MAPK inhibitor and PAF receptor antagonists. PAF-induced up-regulation of PAF-AH levels was solely mediated via the PAF receptor and was p38 MAPK-independent. Conclusion: The proinflammatory mediators, LPS and PAF, increased levels of PAF-AH mRNA via distinct signaling pathways. Springer Basel AG, 2011 PAF acetylhydrolase nationallicence Regulation nationallicence Lipopolysaccharide nationallicence Mitogen activated protein kinase nationallicence PAF receptor nationallicence Howard Katherine Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut Abdel-al Mohammed Department of Chemistry, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut Ditmyer Marcia Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut Patel Nipa Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut Inflammation Research SP Birkhäuser Verlag Basel 60/8(2011-08-01), 735-744 1023-3830 60:8<735 2011 60 11 https://doi.org/10.1007/s00011-011-0326-5 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00011-011-0326-5 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Howard Katherine Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut NATIONALLICENCE 700 1- Abdel-al Mohammed Department of Chemistry, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut NATIONALLICENCE 700 1- Ditmyer Marcia Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut NATIONALLICENCE 700 1- Patel Nipa Department of Biomedical Sciences, University of Nevada Las Vegas School of Dental Medicine, 1001 Shadow Lane, 89106, Las Vegas, Nevada, USA aut NATIONALLICENCE 773 0- Inflammation Research SP Birkhäuser Verlag Basel 60/8(2011-08-01), 735-744 1023-3830 60:8<735 2011 60 11 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer