Figure 1: GFAPCre marks extra- and intrahepatic bile ducts but not HSCs. | Nature Communications

Figure 1: GFAPCre marks extra- and intrahepatic bile ducts but not HSCs.

From: Fate tracing reveals hepatic stellate cells as dominant contributors to liver fibrosis independent of its aetiology

Figure 1

(a) Macroscopic images demonstrate hGFAPCre-induced ZsGreen Cre reporter fluorescence in extrahepatic bile ducts, the brain and brain sections (n=1). (b,c) HSCs were isolated from hGFAPCre mice expressing ZsGreen (n=2) and were either plated (b) or analysed by flow cytometry (c). LratCre mice served as positive control (n=3). (d) HSCs were isolated from hGFAPCre mice expressing mTom/mGFP Cre reporter and plated (n=1). (e) Sections from untreated (n=1), bile duct-ligated (n=1) and CCl4-treated livers (n=2) were stained for desmin, showing no co-localization of ZsGreen and HSC marker desmin by confocal microscopy. (f) Representative western blotting (out of n=3) showing cytokeratin 19 expression but no desmin expression in fluorescence-activated cell sorting-sorted hGFAPCre-labelled ZsGreen-positive cells. (g) hGFAPCre mice undergoing either BDL (n=1) or CCl4 treatment (n=1) show no overlap between tdTomato Cre reporter and Col-GFP reporter, thus excluding a contribution of hGFAPCre-labelled cells to ECM-producing myofibroblasts. (h) Cytokeratin staining of bile duct-ligated hGFAPCre mice shows almost complete overlap of cytokeratin, marking the bile duct proliferates, and hGFAPCre-induced ZsGreen expression (n=1). (i) Sections from untreated mice expressing Cre under the murine Gfap promoter and mTom/mGFP Cre reporter show no GFP expression in the liver. The brain served as the positive control (Inlet). Scale bars, 4 mm (a, left panel), 2 mm (a, upper middle and right panel), 200 μm (a, lower middle and right panel) and 50 μm (b,d,e,g–i).

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