Fig 1

Coculture of LX2 HSCs with high-OPN secreting HepG2 cells induced activation of HSCs while blockade of OPN via APT reverses these effects. Data are presented as mean ± standard deviation of the mean. Coculture of LX2 cells with HepG2 cells caused a significant increase in expression of α-SMA, vimentin, and tenascin-c (all P<0.05) while blockade of OPN expression via APT reversed this effect and expression of all three markers are not significant from LX2 controls (P>0.05). MuAPT did not reverse the effects of HepG2 coculture, and expression of all three markers were significantly increased from LX2 controls (P<0.05). ΔΔCT values were defined using β-actin normalization. n = 3, *P<0.05