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MRNA expression data from livers of wild-type (WT) mice, mice that lack ribosomal protein S6 (Rps6) (DS6), mice that overexpress c-Myc (Myc) and livers that lack Rps6 and also overexpress c-Myc (DS6 Myc)

ABSTRACT: Targeted depletion of ribosomal protein S6 (Rps6) from hepatoblasts of the developing liver results in neonatal sub-lethal hepatic failure due to inhibition of bile duct development and widespread induction of hepatocyte death triggering regeneration. Overexpression of c-Myc is hepatoprotective in the context of Rps6-deficiency and eliminates the need for DS6 livers to regenerate by preventing hepatocyte death. Microarrays were used to identify the transcriptional program associated with loss of hepatic Rps6 and to identify mRNAs associated with c-Myc's hepatoprotective effect in DS6 livers

ORGANISM(S): Mus musculus

PROVIDER: GSE212363 | GEO | 2023/01/04

REPOSITORIES: GEO

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mRNA expression data from livers of wild-type (WT) mice, mice that lack ribosomal protein S6 (Rps6) (DS6), mice that overexpress c-Myc (Myc) and livers that lack Rps6 and also overexpress c-Myc (DS6 Myc)

Project description:mRNA expression data from livers of wild-type (WT) mice, mice that lack ribosomal protein S6 (Rps6) (DS6), mice that overexpress c-Myc (Myc) and livers that lack Rps6 and also overexpress c-Myc (DS6 Myc)

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Ribosomal protein S6 Rps6 heterozygous null deletion effect on footpad epidermis

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Project description:Background/Aim: Legalon SIL (SIL) is a chemically hydrophilized version of silibinin that has exhibited hepatoprotective and antiviral effectiveness against hepatitis C virus (HCV) in patients leading to viral clearance in combination with ribavirin. To elucidate the incompletely understood mode of action of SIL against HCV, we studied viral response kinetics and cellular gene expression during SIL treatment in the absence of an adaptive immune response in uPA-SCID chimeric mice with humanized livers. Methods: Chronically HCV-infected mice were treated with daily intravenous SIL at 469 mg/kg (n=5), 265 mg/kg (n=5) or 61.5 mg/kg (n=5). Serum HCV and human albumin (hAlb) were measured frequently and liver HCV RNA was analyzed at days 3 and 14. Microarray analysis of human hepatocyte gene expression was performed at days 0, 3, and 14 of treatment. Mathematical modeling was used to estimate viral kinetic parameters and SIL effectiveness. Results: While hAlb remained constant, a biphasic viral decline in serum was observed consisting of a rapid 1st phase followed by a 2nd slower (or plateau with the two lower SIL dosing) phase. SIL effectiveness in blocking viral production was similar among dosing groups (median =77%). However, the rate of HCV-infected hepatocyte decline, δ, was dose-dependent. Intracellular HCV RNA levels correlated (r=0.66, P=.01) with serum HCV RNA. Pathway analysis revealed increased anti-inflammatory and anti-proliferative gene expression in human hepatocytes in SIL-treated mice. Conclusions: The results suggest that SIL could lead to a continuous 2nd phase viral decline, i.e., potentially viral clearance, in the absence of adaptive immune response along with increased anti-inflammatory and anti-proliferative gene expression in human hepatocytes.

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