Fig. 4
From: Activation of hepatic stellate cell in Pten null liver injury model
Fibrosis markers are upregulated in the Pten null livers and reduced when Akt2 is simultaneously deleted. a Expression analysis of markers for fibrosis, i.e., desmin, SMAα, Timp 1, Col1a1, and p75NTR are analyzed in 9 (left)- and 12 (right)-month-old Pten control (Con) and null livers (Pm) as well as the Pten/Akt2 double null livers (Dm). Solid bars, Pten null liver; stripped bars, Pten/Akt2 double null; open bars, control liver. Striped bars, Pten/Akt2 double null. *significantly different from controls of the same gene analyzed; **significantly different from Pten null group of the same gene analyzed. n = 5. p < 0.05. Three animals each group are used for the experiment with each sample repeated twice. b Liver tissues were stained with SMAα antibody using indirect immunofluorescence staining (red). The same slides were counterstained with DAPI (blue) to visualize nucleus. Left panels, 9-month-old livers; middle panels, 12-month-old livers; right panels, high mag images of 12-month-old livers. Top panels, control; middle two rows, Pten null; bottom row, Pten and Akt2 double mutant (Pten/Akt2 null). c Immunoblotting analysis of SMAα in liver lysate isolated from the indicated mouse models. Pten control (Con) and null livers (Pm) as well as the Pten/Akt2 double null livers (Dm)