Alterations in the hepatocyte epigenetic landscape in steatosis.

Fatty liver disease or the accumulation of fat in the liver, has been reported to affect the global population. This comes with an increased risk for the development of fibrosis, cirrhosis, and hepatocellular carcinoma. Yet, little is known about the effects of a diet containing high fat and alcohol towards epigenetic aging, with respect to changes in transcriptional and epigenomic profiles.

Kupffer cells are protective in alcoholic steatosis.

Massive accumulation of lipids is a characteristic of alcoholic liver disease. Excess of hepatic fat activates Kupffer cells (KCs), which affect disease progression. Yet, KCs contribute to the resolution and advancement of liver injury.

CRUP: a comprehensive framework to predict condition-specific regulatory units.

We present the software Condition-specific Regulatory Units Prediction (CRUP) to infer from epigenetic marks a list of regulatory units consisting of dynamically changing enhancers with their target genes. The workflow consists of a novel pre-trained enhancer predictor that can be reliably applied across cell types and species, solely based on histone modification ChIP-seq data. Enhancers are subsequently assigned to different conditions and correlated with gene expression to derive regulatory units.

mRNA Binding Protein 2 Transgenic Mice Are More Prone to Develop a Ductular Reaction and to Progress Toward Cirrhosis.

The insulin-like growth factor 2 () mRNA binding proteins (IMPs/IGF2BPs) IMP1 and 3 are regarded as oncofetal proteins, whereas the hepatic IMP2 expression in adults is controversially discussed. The splice variant IMP2-2/p62 promotes steatohepatitis and hepatocellular carcinoma. Aim of this study was to clarify whether IMP2 is expressed in the adult liver and influences progression toward cirrhosis.

The long non-coding RNA suppresses carcinogenesis and chemoresistance in hepatocellular carcinoma.

The long non-coding RNA (lncRNA) represents a maternally expressed and epigenetically regulated imprinted gene product and is discussed to have either tumor-promoting or tumor-suppressive actions. Recently, was shown to be regulated under inflammatory conditions. Therefore, aim of this study was to determine the function of in hepatocellular carcinoma (HCC), an inflammation-associated type of tumor.

Hepatic interleukin-6 production is maintained during endotoxin tolerance and facilitates lipid accumulation.

Gut-derived bacterial endotoxins, such as lipopolysaccharide (LPS), contribute to the pathogenesis of steatosis and steatohepatitis by activating Kupffer cells, the resident liver macrophages. Exposure of macrophages to low doses of LPS causes hyporesponsiveness upon subsequent endotoxin challenge, a phenomenon termed endotoxin or LPS tolerance. In the present study, we aimed to examine whether LPS-induced lipid accumulation is affected by endotoxin tolerance.

Susceptibility of Different Mouse Wild Type Strains to Develop Diet-Induced NAFLD/AFLD-Associated Liver Disease.

Although non-alcoholic and alcoholic fatty liver disease have been intensively studied, concerning pathophysiological mechanisms are still incompletely understood. This may be due to the use of different animal models and resulting model-associated variation. Therefore, this study aimed to compare three frequently used wild type mouse strains in their susceptibility to develop diet-induced features of non-alcoholic/alcoholic fatty liver disease.