Nuclear receptor corepressor 1 deficiency exacerbates asthma by modulating macrophage polarization

被引:1
|
作者
Hou, Chenchen [1 ]
Yan, Lifeng [1 ]
Sun, Ke [2 ]
Zhou, Tianyu [1 ,3 ]
Zou, Yuxin [1 ]
Xiong, Weining [1 ,3 ]
Duan, Sheng-Zhong [4 ,5 ]
机构
[1] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Dept Resp & Crit Care Med, Sch Med, Shanghai 200011, Peoples R China
[2] Fudan Univ, Huashan Hosp, Div Nephrol, Shanghai 200031, Peoples R China
[3] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Sch Med, Shanghai Key Lab Tissue Engn, Shanghai 200011, Peoples R China
[4] Shanghai Jiao Tong Univ, Shanghai Peoples Hosp 9, Lab Oral Microbiota & Syst Dis, Coll Stomatol,Sch Med, Shanghai 200011, Peoples R China
[5] Natl Ctr Stomatol, Natl Clin Res Ctr Oral Dis, Shanghai Key Lab Stomatol, Shanghai 200011, Peoples R China
基金
中国国家自然科学基金;
关键词
INFLAMMATION; REPRESSION; ACTIVATION; ALVEOLAR;
D O I
10.1038/s41420-023-01724-3
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Macrophage polarization plays an important role in asthma. Nuclear receptor corepressor 1 (NCOR1) plays an important role in metabolic and cardiovascular diseases by regulating the function of macrophages. The aim of this research was to examine the role and mechanism of macrophage NCOR1 in the development of asthma. We used ovalbumin (OVA) to induce macrophage NCOR1-deficient mice for asthma formation. Our results revealed that macrophage NCOR1 deficiency markedly enhanced allergic airway inflammation. In addition, NCOR1 deficiency in macrophages was found to enhance M2 polarization. Mechanistic studies suggested that NCOR1 promoted macrophage polarization by interacting with PPAR gamma, contributing to the pathogenesis of asthma. In conclusion, macrophage NCOR1 deficiency promoted the regulation of M2 programming by enhancing PPAR gamma expression to exacerbate asthma. Macrophage NCOR1 might be a potential target for the treatment of asthma.
引用
收藏
页数:9
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