8a) However, in CCl4-treated rat liver sections, there was littl

8a). However, in CCl4-treated rat liver sections, there was little evidence for Selleck PFT�� expression of rPGRMC1 in cells within the scar region other than likely non-specific binding of secondary antibody to occasional inflammatory cells, whereas hepatocytes showed enhanced expression (Fig. 8a and 8b). To firmly establish that rat liver myofibroblasts in vivo do not express rPGRMC1, fibrotic liver sections were co-stained for the expression of α-smooth muscle actin and rPGRMC1. Figure 9b and 9c shows that there was no co-staining of α-smooth muscle

actin in liver myofibroblasts with rPGRMC1, which was restricted to hepatocytes in fibrotic liver sections. Identical staining was obtained in sections from animals treated with CCl4 or CCl4 and 4A3COOHmethyl (data not included). Figure 7 4A3COOHmethyl administration and selleck kinase inhibitor liver fibrosis in a rat CCl 4 model of liver fibrosis. Four animals/group (control or 4A3COOHmethyl) or Smad inhibitor six animals/group (CCl4 or CCl4 + 4A3COOHmethyl) were treated as outlined in the Methods section. Mean and standard deviation serum ALT (a); Mean and standard deviation collagen 1A1 mRNA levels (b); typical views of liver sections stained for sirius red, with a 100 μm scale bar (b); quantitative image analysis for fibrosis

– data are the mean and standard deviation percentage sirius red staining from at least 4 separate animals in each treatment with at least 10 randomly selected fields examined for each animal (c). Figure

8 Rat liver myofibroblast do not express rPGRMC1 Adenosine in vivo – Part A. Low power views (a) and high power views (b) of liver section immunohistochemically stained for rPGRMC1 using IZAb upper panels or identical staining without addition of IZAb (no 1° Ab control) from olive oil control or CCl4 treated animals (note CCl4 + 4A3COOHmethyl treated animals gave similar results). PT, portal tract; CV, central vein; scar, primary location of scar matrix and liver myofibroblasts; ns non-specifically bound secondary antibody. Figure 9 Rat liver myofibroblast do not express rPGRMC1 in vivo – Part B. High powered views show positive staining of non-parenchymal cells in control liver sections (a); co-staining sections from indicated treatment groups – DNA with DAPI (blue), α-sma (green) and PGRMC1 with IZAb (red) with merged panel (b); high powered view of merged liver section from CCl4-treated rat liver (c). PV, periportal venule; PA, periportal arteriole; BD, bile duct. Discussion Steroid hormone interaction with nuclear receptor proteins has been characterized over several decades. Steroids pass through plasma and/or nuclear membranes and interact with intracellular receptor proteins from the steroid/nuclear receptor gene super-family (such as the PXR), representing the canonical (genomic) mode of action for steroid hormone signalling [30].

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