Project description:We performed single cell RNAseq of liver cells in acute liver failure model in mice with different microbiome states to unravel cellular changes in the disease and the impact of gut microbiota on the physiology in this disease.
Project description:Marked enhancement of neutrophil infiltration of the liver is a hallmark of acute liver failure (ALF), a severe life-threatening disease with varying etiologies. However, the mechanisms underlying the regulation of neutrophil entry into the liver and their pathophysiological role during ALF development remain poorly characterized.
Project description:Hepatocyte-derived liver progenitor-like cells (HepLPCs) can reversibly differentiate into mature hepatocytes and play important roles in liver regeneration following acute liver failure. However, the mechanisms by which HepLPCs exert these regulatory effects are unclear. Herein, we report that HepLPCs participate in reinitiating liver regeneration and improving survival during acute liver failure, at least in part, via miRNA-183-5p, which is released from HepLPCs in extracellular vesicles. Thus, these findings may identify novel targets and strategies for the treatment of acute liver failure.
Project description:To explore the potential molecular basis of acute liver failure and identify new therapeutic targets, we performed a transcriptome sequencing analysis of liver samples from acute liver failure mice induced by APAP or TAA toxicity and PBS-treated controls.
Project description:To understand key pathways and regulatory genes in acetaminophen induced Acute Liver Failure (ALF) for pathophysiological and therapeutic mechanisms gene expression was analyzed and significantly up and down regulated genes were identified