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. 2018 Sep 1;370(1):39-45.
doi: 10.1016/j.yexcr.2018.06.008. Epub 2018 Jun 11.

ADAM17/EGFR-dependent ERK activation mediates thrombin-induced CTGF expression in human lung fibroblasts

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ADAM17/EGFR-dependent ERK activation mediates thrombin-induced CTGF expression in human lung fibroblasts

Hui-Yu Chen et al. Exp Cell Res. .

Abstract

Lung fibroblasts play critical roles in fibrotic procedures and contribute to lung fibrosis. Several studies indicated that thrombin, a disintegrin and metalloproteinase 17 (ADAM17), and connective tissue growth factor (CTGF) participate in the formation of pulmonary fibrosis. In this study, we examined the involvement of the ADAM17/epidermal growth factor receptor (EGFR)/extracellular signal-regulated kinase (ERK) pathway in thrombin-stimulated CTGF manifestation in human lung fibroblasts (WI-38). We found that cells treated with thrombin significantly increased ADAM17 expression, ADAM17 and c-Jun phosphorylation in time-dependent manners. Thrombin-stimulated CTGF expression, ERK and c-Jun phosphorylation were inhibited by TAPI-0 (an ADAM17 inhibitor). Moreover, U0126 (an ERK inhibitor) inhibited thrombin-stimulated CTGF expression and c-Jun phosphorylation. Cells transfected with small interfering RNA of the EGFR attenuated thrombin-stimulated ERK phosphorylation, c-Jun phosphorylation, and CTGF expression. Thus, these results suggested that ADAM17/EGFR-dependent ERK activation mediated thrombin-stimulated CTGF expression in human lung fibroblasts.

Keywords: CTGF; EGFR; ERK; Lung fibroblasts; Thrombin.

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