https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15991 Wed 11 Apr 2018 11:51:02 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:15242 Tue 11 Jun 2019 11:55:23 AEST ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11176 Sat 24 Mar 2018 08:14:32 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:11518 Sat 24 Mar 2018 08:10:22 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:22280 in silico and confirmed in luciferase reporter assays. miR-9 function was inhibited with sequence-specific antagomirs. The efficacy of DEX was assessed by quantifying glucocorticoid receptor (GR) cellular localization, protein phosphatase 2A (PP2A) activity, and AHR. Results: Exposure of pulmonary macrophages to IFN-γ/LPS synergistically induced miR-9 expression; reduced levels of its target transcript, protein phosphatase 2 regulatory subunit B (B56) δ isoform; attenuated PP2A activity; and inhibited DEX-induced GR nuclear translocation. Inhibition of miR-9 increased both PP2A activity and GR nuclear translocation in macrophages and restored steroid sensitivity in multiple models of steroid-resistant AHR. Pharmacologic activation of PP2A restored DEX efficacy and inhibited AHR. MiR-9 expression was increased in sputum of patients with neutrophilic but not those with eosinophilic asthma. Conclusion: MiR-9 regulates GR signaling and steroid-resistant AHR. Targeting miR-9 function might be a novel approach for the treatment of steroid-resistant asthma.]]> Sat 24 Mar 2018 07:17:42 AEDT ]]>