Imperial College London
Alternate

DrYoumingZhang

Faculty of Medicine, National Heart & Lung Institute

Lecturer (non-clinical) in Respiratory Genomics
 
 
 
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Contact

 

+44 (0)20 7594 7974y.zhang

 
 
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Location

 

413Guy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Zheng:2022:10.1007/s10753-022-01772-4,
author = {Zheng, Z and Li, J and Cui, Y and Wang, W and Zhang, M and Zhang, Y and Bai, Y and Ying, S and Gao, G},
doi = {10.1007/s10753-022-01772-4},
journal = {Inflammation},
pages = {763--778},
title = {IRAK-M regulates proliferative and invasive phenotypes of lung fibroblasts},
url = {http://dx.doi.org/10.1007/s10753-022-01772-4},
volume = {46},
year = {2022}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Lung fibroblasts play an important role in subepithelial fibrosis, one feature for airway remodeling. IL-1 receptor-associated kinase (IRAK)-M was shown to involve fibrosis formation in airways and lung through regulation of inflammatory responses. IRAK-M is expressed by lung fibroblasts, whether IRAK-M has direct impact on lung fibroblasts remains unclear. In this investigation, we evaluated in vitro effect of IRAK-M on phenotypes of lung fibroblasts by silencing or overexpressing IRAK-M. Murine lung fibroblasts (MLg) were stimulated with house dust mite (HDM), IL-33, and transforming growth factor (TGF) β1. Techniques of small interfering RNA or expression plasmid were employed to silence or overexpress IRAK-M in MLg fibroblast cells. Proliferation, migration, invasiveness, and fibrosis-related events were evaluated. Significant upregulation of IRAK-M expression in MLg cells was caused by these stimuli. Silencing IRAK-M significantly increased proliferation, migration, and invasiveness of lung fibroblasts regardless of stimulating conditions. By contrast, IRAK-M overexpression significantly inhibited proliferation and motility of MLg lung fibroblasts. IRAK-M overexpression also significantly decreased the expression of fibronectin, collagen I, and α-SMA in MLg cells. Under stimulation with TGFβ1 or IL-33, IRAK-M silencing reduced MMP9 production, while IRAK-M overexpression increased MMP9 production. Modulation of IRAK-M expression affected cytokines production, either decreased or increased expression of TNFα and CXCL10 by the cells regardless of stimulation. Our in vitro data reveal that IRAK-M directly impacts on lung fibroblasts through modulation of cellular motility, release of inflammatory, and fibrotic cytokines of lung fibroblasts. These might suggest a new target by regulation of IRAK-M in slowing airway remodeling.
AU  - Zheng,Z
AU  - Li,J
AU  - Cui,Y
AU  - Wang,W
AU  - Zhang,M
AU  - Zhang,Y
AU  - Bai,Y
AU  - Ying,S
AU  - Gao,G
DO  - 10.1007/s10753-022-01772-4
EP  - 778
PY  - 2022///
SN  - 0360-3997
SP  - 763
TI  - IRAK-M regulates proliferative and invasive phenotypes of lung fibroblasts
T2  - Inflammation
UR  - http://dx.doi.org/10.1007/s10753-022-01772-4
UR  - https://link.springer.com/article/10.1007/s10753-022-01772-4
UR  - http://hdl.handle.net/10044/1/102152
VL  - 46
ER  -
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