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ADAM17/EGFR-dependent ERK Activation Mediates Thrombin-Induced CTGF Expression in Human Lung Fibroblasts

ADAM17/EGFR-dependent ERK Activation Mediates Thrombin-Induced CTGF Expression in Human Lung Fibroblasts

Hui-Yu Chen, Chien-Huang Lin, Bing-Chang Chen

Exp Cell Res. 2018 Sep 1;370(1):39-45.

PMID: 29902535

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.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP163958734	TAPI-0		163958-73-4	Price

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