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. Author manuscript; available in PMC: 2015 Apr 1.
Published in final edited form as: Hepatology. 2014 Feb 18;59(4):1435–1447. doi: 10.1002/hep.26790

Figure 4. SDF1α/CXCR4 axis promotes HSC to myofibroblast differentiation in the face of PDGFR blockade by sorafenib.

Figure 4

A, Exposure to recombinant PDGF-B increased HSC proliferation, while treatment with sorafenib reduced the viability of HSCs. Exposure to recombinant SDF1α increased the viability of HSCs despite PDGFR inhibition using sorafenib treatment, in a dose-dependent manner. HSC viability was measured by MTT assay (N=6 experimental repeats). B, Exposure to recombinant SDF1α increased the expression of α-SMA and collagen I and reduced cleaved caspase-3 expression (evaluated by Western blotting) despite sorafenib treatment, in a dose-dependent manner. C, Exposure to recombinant SDF1α increased viability of HSCs despite sorafenib treatment (N=3–5 experimental repeats). D, Exposure to recombinant SDF1α upregulated collagen I and α-SMA expression levels as well as ERK and AKT activation in HSCs, consistent with their myofibroblast differentiation. Inhibition of CXCR4 with AMD3100 (D) or using siRNA (E) prevented the effects of SDF1α. F, ERK inhibition with FR-180204 (2μM) decreased α-SMA expression in HSCs treated with recombinant SDF1α. Data are presented as mean ± SEM.