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The aim of the present study was to determine whether Interleukin   (IL)-1β-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-1β-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 α-smooth   muscle actin (α-SMA) were assessed by either reverse transcription PCR or the   SABC assay. IL-1β-induced-ERK signaling activation in MRC-5 cells was   inhibited by pretreatment with the LNT or ERK inhibitor U0126. IL-1β-enhanced   cell proliferation and expression of FN, Col I and α-SMA were also attenuated   by the treatment with LNT. Our study revealed that activation of ERK   signaling is involved in IL-1β-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

Reversal of il-1β-mediated human embryonic pulmonary fibroblast transdifferentiation by targeting the ERK signaling pathway