Abstract
The aim of the present study was to determine whether Interleukin (IL)-1?-mediated human embryonic pulmonary fibroblast transdifferentiation could be reversed by targeting of the ERK signaling pathway. The human embryonic pulmonary fibroblast MRC-5 cell line was used as a model to observe IL-1?-mediated transdifferentiation as well and the inhibitory effects of lentinan (LNT). Cell proliferation was examined by a CCK-8 assay. ERK signaling activity was detected using immunoblotting with phospho-ERK antibody. The expression levels of fibronectin (FN), Col I and ?-smooth muscle actin (?-SMA) were assessed by either reverse transcription PCR or the SABC assay. IL-1?-induced-ERK signaling activation in MRC-5 cells was inhibited by pretreatment with the LNT or ERK inhibitor U0126. IL-1?-enhanced cell proliferation and expression of FN, Col I and ?-SMA were also attenuated by the treatment with LNT. Our study revealed that activation of ERK signaling is involved in IL-1?-mediated human embryonic pulmonary fibroblast proliferation, phenotypic switching and collagen secretion. These transdifferentiation events in MRC-5 cells could be reversed with LNT treatment by targeting the ERK signaling pathway.
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