MicroRNA-10a-3p mediates Th17/Treg cell balance and improves renal injury by inhibiting REG3A in lupus nephritis

Int Immunopharmacol. 2020 Nov:88:106891. doi: 10.1016/j.intimp.2020.106891. Epub 2020 Aug 24.

Abstract

Background: The therapeutic approaches guided toward microRNAs (miRNAs) have been extensively explored in lupus nephritis (LN), but the precise position of miR-10a-3p posted in disease is not translated thoroughly. Therein, this work pivoting on miR-10a-3p was launched with the involvement of regenerating islet-derived 3 α (REG3A).

Methods: Peripheral blood samples from LN patients and healthy controls (n = 132) were collected. miR-10a-3p and REG3A expression in peripheral blood mononuclear cells were tested. Mice were injected with miR-10a-3p agomir, miR-10a-3p antagomir and/or REG3A low expression vector for presentation of their roles in renal function, T helper cell 17 (Th17)/regulatory cell (Treg) balance, renal pathological damage, JAK2/STAT3 pathway activation and renal injury in LN. The relation between miR-10a-3p and REG3A was tested.

Results: MiR-10a-3p was down-regulated while REG3A was up-regulated in LN. Restoring miR-10a-3p or silencing REG3A decreased Th17/Treg ratio in CD4+ T cells, inhibited JAK2/STAT3 pathway activation, ameliorated renal function, improved renal pathological damage and alleviated renal injury in LN. REG3A depletion negated the effects of down-regulated miR-10a-3p on LN. MiR-10a-3p targeted REG3A.

Conclusion: The work elucidates that miR-10a-3p restoration decreases Th17/Treg ratio and attenuates renal injury in LN via inhibiting REG3A and the activation of JAK2/STAT3 pathway, which renews the therapeutic reference for LN management.

Keywords: Lupus nephritis; MicroRNA-10a-3p; Regenerating islet-derived 3 α; Renal injury; Th17/Tregs balance.

MeSH terms

  • Adult
  • Animals
  • Female
  • Humans
  • Janus Kinase 2 / immunology
  • Kidney / immunology
  • Lupus Nephritis / blood
  • Lupus Nephritis / immunology*
  • Mice, Inbred C57BL
  • MicroRNAs*
  • Middle Aged
  • Pancreatitis-Associated Proteins / genetics
  • Pancreatitis-Associated Proteins / immunology*
  • STAT3 Transcription Factor / immunology
  • Spleen / cytology
  • T-Lymphocytes, Regulatory / immunology*
  • Th17 Cells / immunology*

Substances

  • MIRN10 microRNA, human
  • MicroRNAs
  • Pancreatitis-Associated Proteins
  • REG3A protein, human
  • STAT3 Transcription Factor
  • STAT3 protein, human
  • JAK2 protein, human
  • Janus Kinase 2