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MiR-23a regulates T cellular Redox metabolism in juvenile idiopathic arthritis

ABSTRACT: Juvenile idiopathic arthritis (JIA) is a chronic rheumatic disease with altered transcriptional signatures at the site of inflammation. mRNA transcription and translation are amongst other epigenetic mechanisms tightly regulated by specific miRNA expression. To determine the roles of different miRNAs within JIA pathogenesis we performed a global miRNA expression analysis in parallel in cells from the arthritic joint and peripheral blood of JIA patients, which demonstrates a different composition of miRNA expression at the site of inflammation. Bioinformatic analysis of predicted miRNA target genes suggests a huge overrepresentation of genes involved in metabolic and oxidative stress pathways in the inflamed joint. On the cellular level enhanced reactive oxygen species (ROS) and signs of highly activated metabolism in JIA T cells are present. Despite enhanced ROS levels within the local inflammatory milieu, JIA T cells are hyperproliferative and reveal a TNFa dependent overexpression of miR-23a, which is an inhibitor of PPIF, the regulator of mitochondrial ROS escape. TNFa blockade reduces miRNA-23a, rescues PPIF expression and ROS shuttling and thereby inhibits hyperproliferation. Our data show a novel mechanism of T cell proliferation and metabolism in JIA, which is mediated by miRNA dependent mitochondrial ROS shuttling.

ORGANISM(S): synthetic construct Homo sapiens

PROVIDER: GSE134984 | GEO | 2022/07/26

REPOSITORIES: GEO

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