Fig. 1: GITRL expression is significantly increased in hepatic progenitor cells experiencing epithelial–mesenchymal transition. | Cell Death & Disease

Fig. 1: GITRL expression is significantly increased in hepatic progenitor cells experiencing epithelial–mesenchymal transition.

From: GITR/GITRL reverse signalling modulates the proliferation of hepatic progenitor cells by recruiting ANXA2 to phosphorylate ERK1/2 and Akt

Fig. 1

A The morphology of hepatic progenitor cells and 16-day TGF-β1-treated hepatic progenitor cells. B RNA array and GSEA revealed activation of the hallmarks of epithelial–mesenchymal transition in 16-day TGF-β1-treated hepatic progenitor cells compared to control cells. C Volcano analysis of RNA array data showed that GITRL was the most significantly induced gene in hepatic progenitor cells by fold change. D Heatmap expression levels of GITRL, GITR, and epithelial–mesenchymal transition-related genes in the TGF-β1-treated hepatic progenitor cells and control cells by RNA arrays. E TaqMan RT-PCR analysis showed that TGF-β1 time-dependently induced GITRL and GITR expression in hepatic progenitor cells (N = 3). F Immunofluorescence staining without permeabilization and flow cytometry were used to analyse the expression of GITRL and GITR in the 6-day TGF-β1-treated hepatic progenitor cells. G 3D-SIM images of GITRL expression in the control hepatic progenitor cells and the cells treated by TGF-β1 after immunofluorescence staining without permeabilization.

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