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GATA1 ‐activated lncRNA OIP5 ‐ AS1 and GAS5 promote pyroptosis to exacerbate asthma through regulating miR ‐136‐5p/ LIFR axis

上睑下垂 炎症体 基因敲除 下调和上调 化学 炎症 细胞生物学 生物 免疫学 细胞凋亡 生物化学 基因
作者
Suzhi Zhao,Sini Huang,Yawei Wu,Xiao‐Zhou Yao,Xingjun Cai
出处
期刊:The FASEB Journal [Wiley]
卷期号:38 (22): e70159-e70159 被引量:1
标识
DOI:10.1096/fj.202401186rr
摘要

Pyroptosis plays a pivotal role in airway epithelial inflammation during the progression of asthma. This study aimed to explore the influence and mechanisms of opa-interacting protein 5 antisense RNA1 (OIP5-AS1) and growth arrest-specific transcript 5 (GAS5) on pyroptosis in asthmatic models. Pyroptosis was induced in Dermatophagoides pteronyssinus 1 (Der p1)-exposed 16HBE cells and ovalbumin (OVA)-challenged rats. Subsequently, pyroptosis and its related molecular mechanisms were investigated. Our results indicated that GATA1, OIP5-AS1, GAS5, and LIFR were upregulated, while miR-136-5p was downregulated in the patients and experimental models of asthma. OIP5-AS1/GAS5 knockdown repressed NLRP3 inflammasome-mediated pyroptosis in 16HBE cells. Mechanistically, OIP5-AS1/GAS5 sponged miR-136-5p to enhance LIFR expression and subsequently activated NF-κB pathway. OIP5-AS1, GAS5, or LIFR-mediated induction of pyroptosis was abrogated by miR-136-5p mimics or NF-κB inhibitors (BAY11-7082). Finally, GATA1 transcriptionally activated OIP5-AS1/GAS5 to trigger pyroptosis, thereby driving asthma progression in vivo and in vitro. In conclusion, OIP5-AS1/GAS5 transcriptionally activated by GATA1 promoted NLRP3 inflammasome-mediated pyroptosis via the modulation of miR-136-5p/LIFR/NF-κB axis and consequently resulted in airway inflammation in asthma. Our results may provide novel therapeutic strategies for asthma.
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