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miR-132-3p downregulates FOXO1 in CD4 + T cells and is associated with disease manifestations in patients with lupus.

Authors :
Qin H
Chen S
Liu X
Liang J
Wu H
Zhu X
Source :
The Journal of international medical research [J Int Med Res] 2024 Oct; Vol. 52 (10), pp. 3000605241286762.
Publication Year :
2024

Abstract

Objective: This study aimed to evaluate the expression status of miR-132-3p in CD4 <superscript>+</superscript> T cells in patients with systemic lupus erythematosus (SLE) and explore its potential role in SLE development.<br />Methods: The study included 60 patients with SLE and 30 healthy controls. miR-132-3p expression in CD4 <superscript>+</superscript> T cells was detected by real-time quantitative reverse transcription polymerase chain. Bioinformatics analyses were employed to predict target genes and explore the potential role of miR-132-3p. The associations between miR-132-3p levels and SLE Disease Activity Index (SLEDAI) score, as well as laboratory characteristics, were analyzed.<br />Results: miR-132-3p levels in CD4 <superscript>+</superscript> T cells were significantly higher in patients with SLE compared with healthy controls. Bioinformatics analysis identified FOXO1 as a potential target gene of miR-132-3p, with a particular emphasis on the FOXO signaling pathway. miR-132-3p up-regulation in CD4 <superscript>+</superscript> T cells was associated with high SLEDAI score, high anti-double-stranded DNA levels, low C3 and C4 levels, positive anti-ribosomal P, and high 24-hour urinary protein levels in patients with SLE.<br />Conclusions: miR-132-3p may contribute to CD4 <superscript>+</superscript> T cell dysregulation during SLE by targeting FOXO1 and could potentially be used to assess disease severity.<br />Competing Interests: Declaration of conflicting interestsThe authors declared no potential conflicts of interest.

Details

Language :
English
ISSN :
1473-2300
Volume :
52
Issue :
10
Database :
MEDLINE
Journal :
The Journal of international medical research
Publication Type :
Academic Journal
Accession number :
39429035
Full Text :
https://doi.org/10.1177/03000605241286762