Details

Autor(en) / Beteiligte

• Cai, Yan
• Zhang, Yi
• Wang, Sihan
• Changyong, E.

Titel

MiR-23b-3p alleviates Sjögren's syndrome by targeting SOX6 and inhibiting the NF-κB signaling

Ist Teil von

• Molecular immunology, 2024-08, Vol.172, p.68-75

Ort / Verlag

Elsevier Ltd

Erscheinungsjahr

2024

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• MicroRNA-23b-3p has been demonstrated to act as a safeguard against several autoimmune diseases. However, its role in Sjögren's syndrome (SS) remains unclear. In order to investigate its role in SS, we administered agomiR-23b-3p or agomiR-NC to non-obese diabetic (NOD) mice via tail vein weekly for 6 weeks. The study examined the saliva flow rate, histological changes in submandibular glands, and levels of autoantibodies. Additionally, the levels of several cytokines, cell apoptosis, and NF-κB signaling were evaluated. The protective effect of miR-23b-3p was confirmed in a cell model. The results demonstrated that miR-23b-3p overexpression improved salivary flow rates, inhibited lymphocyte infiltration, reduced cytokine levels, and suppressed cell apoptosis in NOD mice. Moreover, NF-κB signaling was inactivated following miR-23b-3p overexpression. In a cellular model of SS, overexpression of miR-23b-3p protected submandibular gland epithelial cells exposed to IFN-γ against apoptosis and inflammation by targeting SOX6. The study concludes that miR-23b-3p alleviates SS by targeting SOX6 and inhibiting the NF-κB signaling pathway. The miR-23b-3p/SOX6 axis represents a promising avenue for the development of novel therapeutic strategies for SS. •MiR-23b-3p was downregulated in a spontaneous animal model for SS.•MiR-23b-3p attenuated SS in mice by modulating Th1/Th17/Treg cells and cell apoptosis.•MiR-23b-3p overexpression inhibited the NF-κB pathway in NOD mice.•MiR-23b-3p exerted its protective effect by targeting SOX6 in vitro.