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. Author manuscript; available in PMC: 2016 Sep 1.
Published in final edited form as: J Hepatol. 2015 Apr 20;63(3):670–678. doi: 10.1016/j.jhep.2015.04.013

Figure 2. Recombinant Gas6 induces HSC activation via Axl/AKT signaling and Axl deficiency reduces specific traits of HSC transdifferentiation.

Figure 2

A, Axl silencing using specific siRNAs reduced Axl protein expression and HSC activation, quantified as the ratio α-SMA/β-actin at 48 hours post-transfection. (n=3). B, Representative western blot of α-SMA expression in LX2 treated with rGas6 (500 ng/ml) for 0 to 3 days and quantification compared to β-actin content. (n=2). C, Representative western blot of phospho-Axl, phospho-MERTK, phospho-AKT, AKT and β-actin in total extracts, and p65 subunit of NF-κB and laminin in nuclear extracts from LX2 cells after rGas6 administration (500 ng/ml) and incubation with PI3K inhibitor LY294002. (n=2). D, mRNA expression level of α-SMA, Col1a1, TIMP-1 and TGF-β in HSCs from WT and Axl KO mice cultured in vitro for different times, using as β-actin control (n=3). E, Representative western blot of α-SMA, PCNA and MMP9 in protein extracts from WT and Axl KO mice HSCs after 10 days of in vitro culture (n=2). *, P≤0.05, Student’s t test.