Research Paper Volume 15, Issue 23 pp 13854—13864

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

Mingyu Jiang1, , Jicheng Dai1, , Chunming Jiang2, , Yanbo Pan3, , Mingyong Ren1, , Mengnan Xing1, ,

  • 1 Department of Pediatrics, The First Affiliated Hospital of Harbin Medical University, Harbin 150001, P.R. China
  • 2 Department of Neonatology, Zhuhai Women and Children’s Hospital, Zhuhai 519060, P.R. China
  • 3 Department of Neurosurgery, Tieling Central Hospital, Tieling 112000, P.R. China

Received: February 3, 2023       Accepted: October 24, 2023       Published: December 4, 2023      

https://doi.org/10.18632/aging.205266
How to Cite

Copyright: © 2023 Jiang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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.

Abbreviations

STAT3: signal transducer and activator of transcription-3; lncRNA: long noncoding RNA; MEG8: maternally expressed gene 8; RORγt: receptor-related orphan receptor γt; Foxp3: the transcription factor forkhead box P3; HSP: Henoch–Schonlein purpura; Th17 cell: interleukin (IL)-17–secreting T helper cell; Treg cell: CD4+/CD25+ regulatory T cell; RMDMs: rat monocyte–derived macrophages; RIPA: radio immunoprecipitation assay; RA: rheumatoid arthritis; SLE: systemic lupus erythematosus; MAPK: mitogen-activated protein kinase.