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Title: TNF-α-induced NF-κB activation promotes myofibroblast differentiation of LR-MSCs and exacerbates bleomycin-induced pulmonary fibrosis
Authors: Hou, J
Ma, T
Cao, H
Chen, Y
Wang, C
Chen, X
Xiang, Z 
Han, X
Keywords: Idiopathic pulmonary fibrosis (IPF)
Lung resident mesenchymal stem cells (LR-MSCs)
Myofibroblast differentiation
NF-κB signaling
Tumor necrosis factor-α (TNF-α)
Issue Date: 2018
Publisher: John Wiley & Sons
Source: Journal of cellular physiology, 2018, v. 233, no. 3, p. 2409-2419 How to cite?
Journal: Journal of cellular physiology 
Abstract: Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive, and irreversible lung disease of unknown cause. It has been reported that both lung resident mesenchymal stem cells (LR-MSCs) and tumor necrosis factor-α (TNF-α) play important roles in the development of pulmonary fibrosis. However, the underlying connections between LR-MSCs and TNF-α in the pathogenesis of pulmonary fibrosis are still elusive. In this study, we found that the pro-inflammatory cytokine TNF-α and the transcription factor nuclear factor kappa B (NF-κB) p65 subunit were both upregulated in bleomycin-induced fibrotic lung tissue. In addition, we discovered that TNF-α promotes myofibroblast differentiation of LR-MSCs through activating NF-κB signaling. Interestingly, we also found that TNF-α promotes the expression of β-catenin. Moreover, we demonstrated that suppression of the NF-κB signaling could attenuate myofibroblast differentiation of LR-MSCs and bleomycin-induced pulmonary fibrosis which were accompanied with decreased expression of β-catenin. Our data implicates that inhibition of the NF-κB signaling pathway may provide a therapeutic strategy for pulmonary fibrosis, a disease that warrants more effective treatment approaches.
ISSN: 0021-9541
EISSN: 1097-4652
DOI: 10.1002/jcp.26112
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