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. Author manuscript; available in PMC: 2013 Apr 25.
Published in final edited form as: Gastroenterology. 2012 Jun 8;143(3):765–76.e1-3. doi: 10.1053/j.gastro.2012.05.049

Figure 5. Stat3-deficient HSCs have decreased activation.

Figure 5

(A)Upregulation of Stat3, IL-17RA, IL-6RA, OSM-R, and LIF-1-R, but not Stat1 or IL-10Ra/b, was detected in aHSCs in comparison with qHSCs using the whole mouse genome microarray (Suppl. Methods). The mRNA level is the average of the multiple probes (p<0.01).

(B) Development of liver fibrosis is attenuated in GFAPStat3−/− mice compared to wild type Stat3f/f mice. Livers from wild type mice (untreated (n=2), BDL (n=4) and CCl4-treated (n=4)), and GFAPStat3−/− mice (untreated (n=2), BDL (n=5) and CCl4-injured (n=6)), were analyzed by Sirius Red staining, and immunostaining for α-SMA and Desmin, and quantified (as percent of positive area, *p<0.01, **p<0.05). Representative bright field micrographs are shown using × 10 objectives.

(C) Stat3-deficient and wild type primary HSCs were in vitro stimulated with IL-17A (10 ng/ml, 4 h). The ability to activate a-SMA and Col1a1 mRNA, and produce cytokines HGF, TGF-β1, PDGF, IL-6 mRNA was impaired in Stat3−/− HSCs compared to wt HSCs. *p<0.001, **p<0.005, ns - non significant.