The miR-641-STIM1 and SATB1 axes play important roles in the regulation of the Th17/Treg balance in ITP

Bibliographic Details
Title: The miR-641-STIM1 and SATB1 axes play important roles in the regulation of the Th17/Treg balance in ITP
Authors: Hongkai Zhu, Xueqin Ruan, Kexin Zhao, Wenyong Kuang, Sufang Liu, Wenzhe Yan, Xianming Fu, Zhao Cheng, Ruijuan Li, Hongling Peng
Source: Scientific Reports, Vol 14, Iss 1, Pp 1-13 (2024)
Publisher Information: Nature Portfolio, 2024.
Publication Year: 2024
Collection: LCC:Medicine
LCC:Science
Subject Terms: Immune thrombocytopenia (ITP), Th17/Treg balance, microRNA 641 (miR-641), SATB1, STIM1, Medicine, Science
More Details: Abstract Immune thrombocytopenia (ITP) is an autoimmune disease caused by T-cell dysfunction. Recently, several studies have shown that a disturbed Th17/Treg balance contributes to the development of ITP. MicroRNAs (miRNAs) are small noncoding RNA moleculesthat posttranscriptionally regulate gene expression. Emerging evidences have demonstrated that miRNAs play an important role in regulating the Th17/Treg balance. In the present study, we found that miR-641 was upregulated in ITP patients. In primary T cells, overexpression of miR-641 could cause downregulation of its target genes STIM1 and SATB1, thus inducing a Th17 (upregulated)/Treg (downregulated) imbalance. Inhibition of miR-641 by a miR-641 sponge in primary T cells of ITP patients or by antagomiR-641 in an ITP murine model could cause upregulation of STIM1 and SATB1, thus restoring Th17/Treg homeostasis. These results suggested that the miR-641-STIM/SATB1 axis plays an important role in regulating the Th17/Treg balance in ITP.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2045-2322
Relation: https://doaj.org/toc/2045-2322
DOI: 10.1038/s41598-024-61660-9
Access URL: https://doaj.org/article/8b93757099d041abaf1df398b05d307b
Accession Number: edsdoj.8b93757099d041abaf1df398b05d307b
Database: Directory of Open Access Journals
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More Details
ISSN:20452322
DOI:10.1038/s41598-024-61660-9
Published in:Scientific Reports
Language:English