Project description:Global analysis of differentially expressed genes of livers of wild type and IL-4/IL-13-/- two days after carbon tetrachloride treatment. Total RNA obtained from isolated livers from vehicle and carbon tetrachloride administered wild type and IL-4/IL-13-/- mice.
Project description:Global analysis of differentially expressed genes of livers of wild type and IL-4/IL-13-/- two days after carbon tetrachloride treatment.
Project description:Differential gene expression in mice liver after carbon tetrachloride and acetaminophen administration. Livers from control mice were compared with drug treated mice livers at different time points. Keywords: Time-course
Project description:Purpose: The goals of this study are to use NGS-derived liver transcriptome profiling (RNA-seq) and identify differentially expressed genes in regenerating livers that were treated with ethanol and carbon tetrachloride. Methods: Liver mRNA profiles were generated from ethanol/CCl4-treated floxed homozytoes and Ctgf conditional knockout mice by deep sequencing, in duplicate, using Illumina GAIIx. qRT–PCR validation was performed using SYBR Green assay. Results: Ctgf deficiency was associated with 220 downregulated genes and 29 upregulated genes whereas Yap1 null livers had 351 downregulated genes and 287 upregulated genes after ethanol/CCl4 induced liver damage Conclusions: This study provides detailed analysis of liver transcriptomes in absence of Ctgf or Yap1 genes during ethanol/CCl4-induced injury, with biologic replicates, generated by RNA-seq technology.
Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.
Project description:Acute hepatic failure (AHF) usually occurs due to the rapid necrosis of liver cells or serious liver injury induced by a variety of pathogenic factors. We used Rat Genome 230 2.0 microarray to further highlight the rat liver tissues after carbon tetrachloride treatment.
Project description:We conditionally deleted Yap/Taz from hepatocytes prior to induction of acute injury by injection of liver toxin carbon tetrachloride (CCl4).
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide(Dgaln/lps), APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates Dgaln/lps-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against Dgaln/lps-induced hepatocyte injury.
Project description:Acute liver failure is a serious clinical manifestation resulting from sudden liver injury, which can be triggered by various factors. One of the most frequent causes of acute liver failure is excessive ingestion of acetaminophen (APAP), which is known to damage hepatocytes directly by reducing glutathione levels in cells, ultimately leading to hepatocyte death.PGE2 can play a dual role in inflammation, either promoting or inhibiting the inflammatory response, depending on the cell type, local concentration, receptor type, and tissue microenvironment. Early studies have shown that PGE2 significantly alleviated acute liver failure induced by galactosamine/lipopolysaccharide, APAP, and carbon tetrachloride. However, the precise mechanism by which PGE2 alleviates APAP-induced acute liver failure remains unclear. The aim of this study is to investigate the mechanisms underlying the protective effects of PGE2 against APAP-induced hepatocyte injury.
