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Exp Cell Res. 2018 Feb 15;363(2):291-298. doi: 10.1016/j.yexcr.2018.01.019. Epub 2018 Feb 3.

Elongation factor-2 kinase acts downstream of p38 MAPK to regulate proliferation, apoptosis and autophagy in human lung fibroblasts.

Author information

1
Department of Respiratory Medcine (Department of Respiiratory and Critical Care Medcine), Key Cite of National Clinical Research Center for Respiratory Disease. Xiangya Hospital, Central South University, 87 Xiangya Road, Changsha, Hunan, China.
2
Laboratory of Respiratory Disease, Affiliated Hospital of Guilin Medical University, 15 Lequn Road, Guilin, Guangxi, China.
3
Department of Respiratory, Guilin People's Hospital affiliated of Guilin Medical University, 15 Lequn Road, Guilin, Guangxi, China.
4
Department of Respiratory, Guilin People's Hospital affiliated of Guilin Medical University, 12 Wenming Road, Guilin, Guangxi, China. Electronic address: wyni0115@163.com.

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic, fatal and progressive fibro-proliferative lung disease, and fibroblast-to-myofibroblast differentiation is a crucial process in the development of IPF. Elongation factor-2 kinase (eEF2K) has been reported to play an important role in various disease types, but the role of eEF2K in IPF is unknown. In this study, we investigated the role of eEF2K in normal lung fibroblast (NHLF) proliferation, differentiation, apoptosis, and autophagy as well as the interaction between eEF2K and p38 MAPK signaling through in vitro experiments. We found that the inhibition of eEF2K markedly augmented cell proliferation and differentiation, suppressed apoptosis and autophagy, and reversed the anti-fibrotic effects of a p38 MAPK inhibitor. Together, our results indicate that eEF2K might inhibit TGF-β1-induced NHLF proliferation and differentiation and activate NHLF cell apoptosis and autophagy through p38 MAPK signaling, which might ameliorate lung fibroblast-to-myofibroblast differentiation.

KEYWORDS:

Apoptosis; Autophagy; Lung fibroblast; eEF2; eEF2K; p38 MAPK

PMID:
29355493
DOI:
10.1016/j.yexcr.2018.01.019
[Indexed for MEDLINE]
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