Project description:Our project is to explore the molecular subtypes for targeted therapies in Alcoholic Hepatitis (AH). We have found that LCN2 gene expression is markedly induced in AH patients and correlated to the disease severity including portal hypertension. Animal data from microarray experiments show that compared with the wild mice, LCN2 knockout mice are protected from CCl4-induced liver fibrosis. The focus of our current study is to investigate the effect of overexpression of LCN2 on functional changes in hepatocytes. To this end, HepG2 cells and human primary hepatocytes (HPH) were overexpressed human LCN2 gene and samples were analyzed through RNA-sequencing.
Project description:Our project is to explore the molecular subtypes for targeted therapies in Alcoholic Hepatitis (AH). We have found that LCN2 gene expression is markedly induced in AH patients and correlated to the disease severity including portal hypertension. Animal data from microarray experiments show that compared with the wild mice, LCN2 knockout mice are protected from CCl4-induced liver fibrosis. The focus of our current study is to investigate the effect of overexpression of LCN2 on functional changes in hepatocytes. To this end, HepG2 cells and human primary hepatocytes (HPH) were overexpressed human LCN2 gene and samples were analyzed through RNA-sequencing.
Project description:Supporting plasma proteomic data from clinical patients with alcoholic hepatitis in comparison to relevant controls and across treatment time points, baseline, 28/29 days, 12 weeks. Samples were digested with trypsin, labeled with TMT 10-Plex, then analyzed by LC-MS/MS. Data was searched with MS-GF+ using PNNL's DMS Processing pipeline.