Clinical Research Papers:

TNFR/TNF-α signaling pathway regulates apoptosis of alveolar macrophages in coal workers' pneumoconiosis

Qing-Zeng Qian, Xiang-Ke Cao, Hai-Yan Liu, Guo-Ying Zheng, Qing-Qiang Qian and Fu-Hai Shen _

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Oncotarget. 2018; 9:1302-1310. https://doi.org/10.18632/oncotarget.18921

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Qing-Zeng Qian1, Xiang-Ke Cao2, Hai-Yan Liu1, Guo-Ying Zheng1, Qing-Qiang Qian3 and Fu-Hai Shen1

1School of Public Health, North China University of Science and Technology, Tangshan 063000, P.R. China

2College of Life Sciences, North China University of Science and Technology, Tangshan 063000, P.R. China

3Department of Neurology, Tangshan Gongren Hospital Affiliated to North China University of Science and Technology, Tangshan 063000, P.R. China

Correspondence to:

Fu-Hai Shen, email: [email protected]

Keywords: coal mixture workers, coal workers' pneumoconiosis, cumulative dust exposure, alveolar macrophages, apoptosis

Received: July 27, 2016     Accepted: May 23, 2017     Published: July 01, 2017


We explored the role of TNFR/TNF-α signalingin apoptosis among alveolar macrophages (AM) and its relevance to the development of coal workers’ pneumoconiosis (CWP). Purified alveolar macrophages (AMs) were prepared from bronchoalveolar lavage fluid harvested from 366 CWP patients and 120 healthy subjects enrolled inthe study. The purified AMs were then divided into control, SOD, anti-TNFR, TNFR and NFkB inhibitor groups and analyzed for apoptosis usingflow cytometry (sub-diploid peak) and western blotting (Bcl-2, Caspase-3 and Caspase-8 expression). We found thatAM apoptosis washigher amongCWP patients than thehealthycontrols. Expression ofBcl-2, Caspase-3 and Caspase-8 was higher inAMs from CWP patientsthan in those from the controlsand correlated with increased AM apoptosis. Univariate and multivariate analyses suggested that CWP grade, initial exposure time, exposure time inyears, and CWP onset agewereall associated with altered levels of Bcl-2, Caspase-3 and Caspase-8. Inhibition of TNFR/TNF-α signaling usinganti-TNFR antibody, SOD or NFkB inhibitionreduced AM apoptosisand decreased Bcl-2, Caspase-3 and Caspase-8 expression. These data suggestinhibition of a TNFR/TNF-α signaling pathway is a potentiallyeffective means ofalleviating CWP by inhibiting AM apoptosis.

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