MiR-223-3p attenuates M1 macrophage polarization via suppressing the Notch signaling pathway and NLRP3-mediated pyroptosis in experimental autoimmune uveitis

上睑下垂 葡萄膜炎 巨噬细胞极化 Notch信号通路 免疫学 炎症体 发病机制 信号转导 自身免疫 细胞生物学 炎症 医学 癌症研究 生物 化学 巨噬细胞 免疫系统 生物化学 体外
作者
Ruyi Qu,Yuan Peng,Mengxian Zhou,Shuqin Xu,Xuewei Yin,Yan Qiu,Bin Liu,Yane Gao,Hongsheng Bi,Dadong Guo
出处
期刊:European Journal of Pharmacology [Elsevier BV]
卷期号:960: 176139-176139 被引量:6
标识
DOI:10.1016/j.ejphar.2023.176139
摘要

Autoimmune uveitis is an intraocular inflammatory disease with a high blindness rate in developed countries such as the United States. It is pressing to comprehend the pathogenesis of autoimmune uveitis and develop novel schemes for its treatment. In the present research, we demonstrated that the Notch signaling pathway was activated, and the level of miR-223-3p was significantly reduced in rats with experimental autoimmune uveitis (EAU) compared with the level of normal rats. To investigate the relationship between miR-223-3p and Notch signaling, EAU rats received miR-223-3p-carrying lentivirus, miR-223-3p vector-carrying lentivirus (miR-223-3p-N), and γ-secretase inhibitor (DAPT), respectively. The results of Q-PCR, immunological experiments, and flow cytometry analysis all support the hypothesis that both miR-223-3p and DAPT, a Notch signaling pathway inhibitor, had similar inhibitory effects on the EAU pathological process. That is to say, they could both inhibit the activation of the Notch signaling pathway via modulating recombination signal binding protein-Jκ (RBPJ) to restore the polarization imbalance of M/M2 macrophages in EAU rats. In addition, miR-223-3p could also inhibit NLRP3 inflammasome activation and inflammasome-induced pyroptosis in ocular tissues. Taken together, our findings indicate that miR-223-3p serves as an important regulator in M1 macrophage polarization and pyroptosis, thereby alleviating the inflammatory response in uveitis.
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