MiR-379-5p aggravates experimental autoimmune uveitis in mice via the regulation of SEMA3A

• Autors principals: Mohan Li (Autor), Xiang Gao (Autor), Kou Liu (Autor), Ning Bao (Autor), Zhengxuan Jiang (Autor)
• Format: Llibre
• Publicat: Taylor & Francis Group, 2021-07-01T00:00:00Z.
• Matèries: article
• Accés en línia: Connect to this object online.
• Notes: 0891-6934; 1607-842X; 10.1080/08916934.2021.1931841
• Keywords: mir-379-5p; sema3a; experimental autoimmune uveitis; Internal medicine; RC31-1245
• Source: Autoimmunity, Vol 54, Iss 5, Pp 275-283 (2021)

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.