Fig. 6: GITR inhibits the proliferation of TGF-β1-induced GITRL-expressing hepatic progenitor cells. | Cell Death & Disease

Fig. 6: GITR inhibits the proliferation of TGF-β1-induced GITRL-expressing hepatic progenitor cells.

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

Fig. 6

A GITRL expression was induced by treatment with TGF-β1 for 6 days in hepatic progenitor cells. GITR-Fc showed a dose-dependent suppression of cell viability of the GITRL-expressing cells, as demonstrated by MTT assays, but did not inhibit the growth of the control cells (N = 4). B Cell growth was monitored and recorded every 1 h for 140 h by the xCELLigence growth curve, showing that GITR-Fc had no effects on the growth of control hepatic progenitor cells but significantly inhibited the growth of the TGF-β1-pretreated hepatic progenitor cells (N = 3). The normalised cell index showed a significant difference at 133 h. C TGF-β1 treatment enhanced the phosphorylation of ERK1/2 (Thr202/Tyr204) and Akt (Ser473) in the hepatic progenitor cells compared to the nontreated control cells, while GITR-Fc reduced the phosphorylation of ERK1/2 (Thr202/Tyr204) and Akt (Ser473) in the TGF-β1-treated cells (N = 3). D The xCELLigence growth curve showed that GITR-Fc inhibited the growth of the TGF-β1-treated nonspecific gRNA-transfected control cells but had no effects on the growth of the TGF-β1-treated GITRL-knockout cells (N = 3). The normalised cell index showed a significant difference at 100 h. E Knocking out GITRL reduced ERK1/2 (Thr202/Tyr204) and Akt (Ser473) phosphorylation, and the GITR-Fc-medicated reduction of ERK1/2 (Thr202/Tyr204) and Akt (Ser473) phosphorylation was not as significant as TGF-β1-treated nonspecific gRNA-transfected control cells.

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