MiR-1165-3p Suppresses Th2 Differentiation via Targeting IL-13 and PPM1A in a Mouse Model of Allergic Airway Inflammation

• DOI: 10.4168/aair.2020.12.5.859
• Publication Date: 2020-07-06T00:55:40Z
• Authors: Zhengxia Wang; Ningfei Ji; Zhongqi Chen; Zhixiao Sun; Chaojie Wu; Wenqing Yu; Fan Hu; Mao Huang; Mingshun Zhang
• Keywords: Allergic Inflammation; Pathogenesis

CD4⁺T cells are essential in the pathogenesis of allergic asthma. We have previously demonstrated that microRNA-1165-3p (miR-1165-3p) was significantly reduced T-helper type (Th) 2 and miR-1165-3p a surrogate marker for atopic Little is known about mechanisms regulation Th2-dominated inflammation. aimed to investigate associations between Th2 differentiation miR-1165b-3p asthma as well possible mechanisms.CD4⁺ naïve T were differentiated into Th1 or vitro. MiR-1165-3p up-regulated down-regulated using lentiviral systems during Th1/Th2 differentiation. In vivo, particles with enhancer administered by tail vein injection on first day house dust mite -induced airway inflammation model. Allergic routinely monitored. To potential targets miR-1165-3p, biotin-microRNA pull-down products sequenced, candidates further verified dual-luciferase reporter assay. The roles target protein phosphatase, Mg2+/Mn2+-dependent 1A (PPM1A), cell explored. Plasma PPM1A determined ELISA 18 subjects 20 controls.The lentivirus encoding suppressed Th2-cell contrast, silencing promoted development. HDM-induced model inflammation, up-regulation accompanied hyper-responsiveness, serum immunoglobulin E, polarization. IL-13 direct miR-1165-3p. expression inversely correlated regulated signal transducer activator transcription AKT signaling pathways Moreover, plasma increased asthmatic patients.MiR-1165-3p negatively may regulate targeting