Figure 7. A1 expression is induced in phagocytosing hepatic stellate cells.

(A) LX-2 cells were exposed to AB in the presence or absence of LY294002, or AG490. Western blot analysis was done to study the anti apoptotic protein, A1 expression. (B) The quantitative densitometry analysis shows that phagocytosis of AB upregulated A1 expression (1.7±0.2-fold), and this was inhibited by blocking the PI3K activity. Inhibiting the JAK pathway however, had only a modest effect on A1 expression N=4, *p<0.05. To study the anti-apoptotic effect of A1, primary rat HSC were transfected with A1 siRNA (30 nM) and exposed to AB. (C) Western blot analysis shows the inhibition of A1 expression by the siRNA. (D) Primary HSC were transfected with either scrambled (Scr) or A1 siRNA (A1si), exposed to AB, in the presence or absence of FasL and cycloheximide. Caspase-3/DAPI staining was performed to assess apoptosis. In the Scr+AB group the apoptosis was (14.1%±0.8). This was increased by FasL and CHX (29.6%±1.2). A1 siRNA transfection induced higher apoptosis rate at baseline (only AB-exposed cells) and after FasL/CHX treatment (42.1%±0.7). Mean±SED, N=4, *p<0.001, **p<0.005.