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image of GLI3 is Inhibited by miR-143-3p and Attenuates Septic-induced Lung Injury and Inflammation by Targeting SFRP1

Abstract

Objectives

Transcription factors (TF) are the central regulatory hubs of signaling pathways in eukaryotic cells. Here, we explored the abnormal expression of TF in septic-induced lung injury by sequencing.

Methods

The levels of target proteins were detected using Western Blot and Elisa. Cell function was evaluated using CCK8 and transwell assays. A double luciferase reporter assay was performed to detect interactions between target molecules.

Results

We found that TF () was abnormally low expressed in a lipopolysaccharide (LPS) induced acute lung injury (ALI) cell model. In an model, overexpression promoted the proliferation and migration and inhibited apoptosis of lung epithelial cells in LPS-induced inflammatory environment. Importantly, overexpression inhibited the secretion of inflammatory factors IL-1β, IL-6, and TNF-α. Additionally, miR-143-3p inhibited the expression of . MiR-143-3p inhibitor alleviated the cell damage caused by LPS, while knocking down this effect, indicating that miR-143-3p downregulated and inhibited its anti-inflammatory effect. () was upregulated in LPS-treated cells and promoter interacted with , suggesting that was a target of TF . Co-transfection with knockdown and overexpression plasmids attenuated the secretion of inflammatory factors IL-1β, IL-6, and TNF-α caused by knockdown in LPS-treated cells, indicating that plays an anti-inflammatory role as a target in the ALI cell model.

Conclusions

miR-143-3p caused degradation of mRNA and thus inhibited the transcription of , leading to decreased proliferation and increased levels of inflammatory factors, providing new potential targets for the clinical diagnosis and treatment of ALI.

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2025-03-10
2025-03-28
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  • Article Type:
    Research Article
Keywords: miR-143-3p ; Septic lung injury ; miRNA ; LPS ; transcription factor
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