DOI: 10.1002/ame2.12523
Deficiency of DEK proto-oncogene alleviates allergic rhinitis by inhibiting RhoA/Ezrin-mediated mitochondrial fission
Longzhu Dai1
Yongde Jin2
Jingmei Chai3
Jianing Yang1
Jiangang Wang1
Mu Chen2
Liangchang Li1
Chongyang Wang1
Guanghai Yan1
1.Jilin Key Laboratory for Immune and Targeting Rese2.Jilin Key Laboratory for Immune and Targeting Rese3.Jilin Key Laboratory for Immune and Targeting Rese
摘要：Background:Allergic rhinitis(AR)is a kind of immune disease mediated by IgE.We are intrigued by the potential role of DEK proto-oncogene(DEK)in inflammation-related diseases.We investigated the effects and mechanisms of DEK in treating AR,aiming to identify potential new treatment targets for AR.
Methods:The AR mouse model was induced by house dust mite(HDM)(1mg/mL).HNEpCs stimulated by HDM(1mg/mL)were pretreated for 24h with or without DEK lentivirus.The effect of DEK knockout or knockdown on AR was evaluated in vitro and in vivo using western blotting,ELISA,flow cytometry,real-time quan-titative PCR,immunohistochemistry,HE staining,PAS staining,Diff staining,and immunofluorescence.
Results:After DEK knockdown,the inflammatory response of AR mice was reduced.In addition,DEK deletion mitigated nasal tissue damage and mitochondrial division.Our further studies showed that DEK deletion or inhibition led to the down-regulation of RhoA activity and decreased phosphorylation of Ezrin and Drp1 proteins,and inhib-ited mitochondrial division.Overall,DEK deficiency mitigated AR by down-regulating RhoA/Ezrin/Drp1 pathway activity.
Conclusion:DEK alleviates AR through RhoA/Ezrin/Drp1 signaling pathway,which provides a new perspective for developing improved therapies and understanding the pathogenesis of AR.
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论文发表日期：2025-11-30
在线出版日期：2026-01-09（本平台首次上网日期，不代表文献的发表时间）
页数：13( 1947-1959 )
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