Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation

Abstract Background Uveitis is a common recurrent autoimmune disease that seriously endangers the visual health of patients. MicroRNAs (miRNAs) are closely related to a series of autoimmune diseases. Methods The present study aimed to investigate the effect of miR-30b-5p on experimental autoimmune u...

Full description

Saved in:
Bibliographic Details
Main Authors: Xuewei Yin, Huixia Wei, Lijie Guo, Bin Liu, Yuan Peng, Mengxian Zhou, Yan Qiu, Ruyi Qu, Yane Gao, Qiuxin Wu, Wenjun Jiang, Hongsheng Bi, Dadong Guo
Format: Article
Language:English
Published: BMC 2025-04-01
Series:Journal of Translational Medicine
Subjects:
Online Access:https://doi.org/10.1186/s12967-025-06438-x
Tags: Add Tag
No Tags, Be the first to tag this record!
_version_ 1850183948789874688
author Xuewei Yin
Huixia Wei
Lijie Guo
Bin Liu
Yuan Peng
Mengxian Zhou
Yan Qiu
Ruyi Qu
Yane Gao
Qiuxin Wu
Wenjun Jiang
Hongsheng Bi
Dadong Guo
author_facet Xuewei Yin
Huixia Wei
Lijie Guo
Bin Liu
Yuan Peng
Mengxian Zhou
Yan Qiu
Ruyi Qu
Yane Gao
Qiuxin Wu
Wenjun Jiang
Hongsheng Bi
Dadong Guo
author_sort Xuewei Yin
collection DOAJ
description Abstract Background Uveitis is a common recurrent autoimmune disease that seriously endangers the visual health of patients. MicroRNAs (miRNAs) are closely related to a series of autoimmune diseases. Methods The present study aimed to investigate the effect of miR-30b-5p on experimental autoimmune uveitis (EAU) and its role in Notch signal activation as well as T helper (Th) cell differentiation, the relationship between miR-30b-5p levels and Notch signal activation, as well as Th cell differentiation in uveitis was further explored through flow cytometry, Immunohistochemistry immunofluorescence staining, PCR Array, and Ingenuity Pathway Analysis, and other technical methods to determine the fidelity of miR-30b-5p strategies in treating uveitis in vivo and in vitro. Results We demonstrated that ocular inflammation was significantly alleviated in EAU rats after miR-30b-5p intervention. miR-30b-5p could effectively inhibit Notch signaling activation and Th17 cell differentiation both in vitro and in vivo, and the Th17/Treg ratios were also notably decreased. Moreover, both Notch signaling and Th17 activation pathways were enriched and activated, in which Notch1 was the upstream regulatory molecule of Dll4 and IL-10 was an up-regulated upstream regulatory network molecule. Furthermore, miR-30b-5p could significantly reduce apoptosis in vitro, and clinical in vitro cell studies have shown that inactivating Notch pathway can improve the imbalance of Th17/Treg and cell apoptosis in T lymphocytes of patients with uveitis. Conclusions Together these studies identify that miR-30b-5p can significantly inhibit Notch signaling activation and Th17 cell differentiation, thereby restoring the Th17/Treg balance to treat uveitis, which may provide new insights into treating uveitis using miRNA interfering strategies. Graphical Abstract
format Article
id doaj-art-e16e0170602a4c558cf37ca7e3511c2e
institution OA Journals
issn 1479-5876
language English
publishDate 2025-04-01
publisher BMC
record_format Article
series Journal of Translational Medicine
spelling doaj-art-e16e0170602a4c558cf37ca7e3511c2e2025-08-20T02:17:10ZengBMCJournal of Translational Medicine1479-58762025-04-0123112210.1186/s12967-025-06438-xTherapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activationXuewei Yin0Huixia Wei1Lijie Guo2Bin Liu3Yuan Peng4Mengxian Zhou5Yan Qiu6Ruyi Qu7Yane Gao8Qiuxin Wu9Wenjun Jiang10Hongsheng Bi11Dadong Guo12Shandong University of Traditional Chinese MedicineAffiliated Eye Hospital of Shandong University of Traditional Chinese MedicineGuangzhou Laboratory, Guangzhou Medical UniversityShandong University of Traditional Chinese MedicineShandong University of Traditional Chinese MedicineShandong University of Traditional Chinese MedicineShandong University of Traditional Chinese Medicine Second Affiliated HospitalShandong University of Traditional Chinese MedicineAffiliated Eye Hospital of Shandong University of Traditional Chinese MedicineAffiliated Eye Hospital of Shandong University of Traditional Chinese MedicineShandong Academy of Eye Disease Prevention and Therapy, Medical College of Optometry and Ophthalmology, Shandong University of Traditional Chinese MedicineAffiliated Eye Hospital of Shandong University of Traditional Chinese MedicineShandong Provincial Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Therapy of Ocular DiseasesAbstract Background Uveitis is a common recurrent autoimmune disease that seriously endangers the visual health of patients. MicroRNAs (miRNAs) are closely related to a series of autoimmune diseases. Methods The present study aimed to investigate the effect of miR-30b-5p on experimental autoimmune uveitis (EAU) and its role in Notch signal activation as well as T helper (Th) cell differentiation, the relationship between miR-30b-5p levels and Notch signal activation, as well as Th cell differentiation in uveitis was further explored through flow cytometry, Immunohistochemistry immunofluorescence staining, PCR Array, and Ingenuity Pathway Analysis, and other technical methods to determine the fidelity of miR-30b-5p strategies in treating uveitis in vivo and in vitro. Results We demonstrated that ocular inflammation was significantly alleviated in EAU rats after miR-30b-5p intervention. miR-30b-5p could effectively inhibit Notch signaling activation and Th17 cell differentiation both in vitro and in vivo, and the Th17/Treg ratios were also notably decreased. Moreover, both Notch signaling and Th17 activation pathways were enriched and activated, in which Notch1 was the upstream regulatory molecule of Dll4 and IL-10 was an up-regulated upstream regulatory network molecule. Furthermore, miR-30b-5p could significantly reduce apoptosis in vitro, and clinical in vitro cell studies have shown that inactivating Notch pathway can improve the imbalance of Th17/Treg and cell apoptosis in T lymphocytes of patients with uveitis. Conclusions Together these studies identify that miR-30b-5p can significantly inhibit Notch signaling activation and Th17 cell differentiation, thereby restoring the Th17/Treg balance to treat uveitis, which may provide new insights into treating uveitis using miRNA interfering strategies. Graphical Abstracthttps://doi.org/10.1186/s12967-025-06438-xExperimental autoimmune uveitisNotch signaling pathwaymiR-30b-5pTh cellNotch1Dll4
spellingShingle Xuewei Yin
Huixia Wei
Lijie Guo
Bin Liu
Yuan Peng
Mengxian Zhou
Yan Qiu
Ruyi Qu
Yane Gao
Qiuxin Wu
Wenjun Jiang
Hongsheng Bi
Dadong Guo
Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
Journal of Translational Medicine
Experimental autoimmune uveitis
Notch signaling pathway
miR-30b-5p
Th cell
Notch1
Dll4
title Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
title_full Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
title_fullStr Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
title_full_unstemmed Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
title_short Therapeutic effect of miR-30b-5p-loaded lentivirus on experimental autoimmune uveitis via inhibiting Notch signaling activation
title_sort therapeutic effect of mir 30b 5p loaded lentivirus on experimental autoimmune uveitis via inhibiting notch signaling activation
topic Experimental autoimmune uveitis
Notch signaling pathway
miR-30b-5p
Th cell
Notch1
Dll4
url https://doi.org/10.1186/s12967-025-06438-x
work_keys_str_mv AT xueweiyin therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT huixiawei therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT lijieguo therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT binliu therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT yuanpeng therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT mengxianzhou therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT yanqiu therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT ruyiqu therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT yanegao therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT qiuxinwu therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT wenjunjiang therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT hongshengbi therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation
AT dadongguo therapeuticeffectofmir30b5ploadedlentivirusonexperimentalautoimmuneuveitisviainhibitingnotchsignalingactivation