Abstract
Uveitis is a disease resulting in the inflammation of uveal tracts, but the factors resulting in uveitis is still obscure. Previous studies have shown that miR-379-5p was involved in the pathogenesis of several diseases, however, the role and regulatory mechanism of miR-379-5p in uveitis were unclear. In our study, we established experimental autoimmune uveitis (EAU) mouse models to explore the role of miR-379-5p in uveitis. RT-qPCR identified that miR-379-5p level was increased in serum of EAU mice. In mechanism, SEMA3A 3’UTR was proven to be directly targeted by miR-379-5p and SEMA3A expression was negatively regulated by miR-379-5p in CD4+ T cells. Moreover, ELISA analysis revealed that knockdown of miR-379-5p suppressed the production of inflammation cytokines including IL-17, TNF-α and IL-β in vitro. These results were reversed by SEMA3A overexpression. In addition, the reduction of Th17 cells under miR-379-5p inhibitor was neutralised by SEMA3A knockdown in vitro. Furthermore, we demonstrated that knockdown of miR-379-5p significantly reversed the increased clinical scores and inflammatory response resulting from EAU treatment and this effect was further countervailed by SEMA3A silencing. Our study suggested that miR-379-5p aggravated uveitis in EAU mice via the regulation of SEMA3A, which may provide a novel insight for uveitis treatment.
Correction Statement
This article has been corrected with minor changes. These changes do not impact the academic content of the article.
Disclosure statement
No potential conflict of interest was reported by the author(s).
Data availability statement
The datasets used or analysed during the current study are available from the corresponding author on reasonable request.