Long noncoding RNA MEG8 induces an imbalance of Th17/Treg cells through the miR-107/STAT3 axis in Henoch-Schonlein purpura rats

Abstract

T-helper (Th) 17/ T-regulatory (Treg) cell dysregulation underlies the pathogenesis of Henoch-Schonlein purpura (HSP). This research focused on the implication/s of the long noncoding RNA (lncRNAs) maternally expressed gene 8 (MEG8) in Th17 and Treg cell differentiation in HSP rats. MEG8, miR-107, signal transducer and activator of transcription-3 (STAT3), receptor-related orphan receptor γt (RORγt), and the transcription factor forkhead box P3 (Foxp3) expression levels were detected using real-time quantitative polymerase chain reaction and Western blot analyses. Flow cytometry was employed for measuring Th17 and Treg cells within the CD4+ T cell population. The interaction between miR-107 and MEG8 or STAT3 was examined. A low proportion of MEG8 and Treg cells together with Th17 cells were denoted within HSP rats. Moreover, MEG8 overexpression altered the Th17/Treg imbalance in peripheral blood CD4+ T-cell population, and the miR-107 mimic and STAT3 silencing reversed this effect. Thus, MEG8 served as a sponge for miR-107, lowering binding activity to STAT3 and thus overexpressing the molecule. Taken together, MEG8 induces an imbalance of Th17/Treg cells through the miR-107/STAT3 axis in HSP rats.