MicroRNA-155 Inhibition Activates Wnt/β-Catenin Signaling to Restore Th17/Treg Cell Balance and Protect against Acute Ischemic Stroke

Acute ischemic stroke (AIS) is a severe Neurological Disease associated with Th17/Treg cell imbalance and dysregulation of the Wnt/β-catenin signaling pathway. This study investigates whether miR-155 inhibition can activate Wnt/β-catenin signaling, improve Th17/Treg balance, and provide neuroprotection against stroke. We conducted a multilevel experimental design, including high-throughput Sequencing, bioinformatics analysis, in vivo mouse models, and in vitro cell experiments. High-throughput Sequencing revealed significant differential gene expression between the miR-155 antagomir-treated and control groups (BioProject: PRJNA1152758). Bioinformatics analysis identified key genes linked to Wnt/β-catenin signaling and Th17/Treg imbalance. In vitro experiments confirmed that miR-155 inhibition activated Wnt/β-catenin signaling and improved Th17/Treg ratios. In vivo studies demonstrated that miR-155 antagomir treatment provided significant neuroprotection against AIS. These findings suggest that targeting miR-155 could be a promising therapeutic strategy for stroke by modulating immune balance and key signaling pathways.

Th17/Treg; Wnt/β-catenin; bioinformatics; ischemic stroke; miR-155.