Transcriptomic analysis of the livers of Bnc2 heterozygous or wild-type mice fed with a pro-fibrogenic NASH diet
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA769442 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The Ayu21-18 mouse line (B6;CBA-Bnc2Gt(pU21)18Imeg/Orl; Infrafrontier EM-05043) was used to generate mice with heterozygous inactivation of Bnc2,which were compared to their wild-type (WT) littermates. Mice were fed a pro-fibrogenic NASH diet for 7.5 weeks and livers were used used to prepare RNA.
2022-08-07 | GSE185527 | GEO
Project description:BACKGROUND & AIMS: Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. METHODS: Microarray was performed to identify differentially expressed genes in NASH. Quantitative real time PCR (qRT-PCR) was used to examine gene expression levels. Western blotting and immunofluorescence staining were employed to examine hemoglobin proteins. Flow cytometry was used to measure intracellular oxidative stress. RESULTS: Analysis of microarray gene expression data has revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopspies from NASH patients. Increased hemoglobin expression in NASH was validated by qRT-PCR. However, the expression of erythrocyte specific marker genes such as SPTA, SPTB, GYPA, GATA1, and ALAS2 did not change, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, induced a dose dependent increase in HBA1 expression in HepG2 cells. Intriguingly, forced hemoglobin expression suppressed oxidative stress. CONCLUSIONS: Oxidative stress upregulates hemoglobin expression in hepatocytes. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage. These findings suggest that hemoglobin is an inducible antioxidant in hepatocytes in response to increased oxidative stress as found in NASH livers. Twelve biopsy diagnosed NASH patients were included in this study. For control groups, total RNA from 5 different subjects were purchased from ADMET. These subjects are free from liver disease.
2010-10-20 | E-GEOD-24807 | biostudies-arrayexpress
Project description:scRNAseq of DIO-NASH mouse livers
| PRJNA664408 | ENA
Project description:BACKGROUND & AIMS: Recent studies revealed that hemoglobin is expressed in some non-erythrocytes and it suppresses oxidative stress when overexpressed. Oxidative stress plays a critical role in the pathogenesis of non-alcoholic steatohepatitis (NASH). This study was to investigate whether hemoglobin is expressed in hepatocytes and how it is related to oxidative stress in NASH patients. METHODS: Microarray was performed to identify differentially expressed genes in NASH. Quantitative real time PCR (qRT-PCR) was used to examine gene expression levels. Western blotting and immunofluorescence staining were employed to examine hemoglobin proteins. Flow cytometry was used to measure intracellular oxidative stress. RESULTS: Analysis of microarray gene expression data has revealed a significant increase in the expression of hemoglobin alpha (HBA1) and beta (HBB) in liver biopspies from NASH patients. Increased hemoglobin expression in NASH was validated by qRT-PCR. However, the expression of erythrocyte specific marker genes such as SPTA, SPTB, GYPA, GATA1, and ALAS2 did not change, indicating that increased hemoglobin expression in NASH was not from erythropoiesis, but could result from increased expression in hepatocytes. Immunofluorescence staining demonstrated positive HBA1 and HBB expression in the hepatocytes of NASH livers. Hemoglobin expression was also observed in human hepatocellular carcinoma HepG2 cell line. Furthermore, treatment with hydrogen peroxide, a known oxidative stress inducer, induced a dose dependent increase in HBA1 expression in HepG2 cells. Intriguingly, forced hemoglobin expression suppressed oxidative stress. CONCLUSIONS: Oxidative stress upregulates hemoglobin expression in hepatocytes. Suppression of oxidative stress by hemoglobin could be a mechanism to protect hepatocytes from oxidative damage. These findings suggest that hemoglobin is an inducible antioxidant in hepatocytes in response to increased oxidative stress as found in NASH livers.
2010-10-21 | GSE24807 | GEO
Project description:Single-Cell Analysis of NASH mouse livers
| PRJNA895847 | ENA
Project description:Comparison between livers of FLS mice and livers of DS (DD shionogi) mice We used FLS mice as model animals of human NASH, while DS mice as control animals. FLS mice develops NASH spontaneously. DS mouse strain is a sister strain of the FLS mouse strain. We compared RNA from pooled livers of three FLS mice and three DS mice at 19 weeks. NASH in livers from FLS mice was confirmied pathologically while simple steatosis of DS mouse livers confirmed.
2013-03-30 | E-GEOD-45624 | biostudies-arrayexpress
Project description:To investigate the function of read-through circRNAs in liver, we obtained human NASH liver tissues and normal liver tissues patients without NAFLD undergoing surgery for hepatic hemangioma.Patients with positive hepatitis B surface antigen or anti-hepatitis C virus (HCV) antibody with detectable HCV RNA, excessive alcohol consumption (20 g/day in men or 10 g/day in women), secondary fatty liver (e.g., use of systemic steroids or tamoxifen), or malignancies before baseline were excluded. We then performed exome capture mRNA sequencing using livers from three NASH patients and three patients with hepatic hemangioma.
2022-09-08 | GSE212741 | GEO
Project description:RNA Sequencing Facilitates Quantitative Analysis of Humanized Normal Livers, NASH Livers, and HCC Transcriptomes
| PRJNA847988 | ENA
Project description:LX2 cells were used for BNC2 and H3K27ac ChIP-seq as well as for CoP-seq
2022-08-07 | GSE185528 | GEO
Project description:Isolated H2KB peptides from control and NASH livers from LDLRKO and Sucrose fed mice.
2023-11-27 | MSV000093515 | MassIVE