Altered miRNA expression in liver and serum of NASH mice
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ABSTRACT:
PROVIDER: PRJNA1057155 | ENA |
REPOSITORIES: ENA
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Project description:Non-alcoholic steatohepatitis (NASH) is a fatty liver disease that does not involve alcohol consumption and is characterized by fatty degeneration, inflammation, and hepatocellular damage. Therefore, predicting future fibrosis is necessary in the early stages of NASH to prevent developing diseases. This study examined histological changes in the liver as well as microRNA expression changes in the liver and serum of NASH mice model to search for potential biomarker candidates that may predict early fibrosis. This study used 6-week-old C57BL/6NJcl male mice and fed the control and NASH groups with a food-breeding solid diet (CE-2) and a high-fat diet (choline-deficient high-fat and 0.1% [w/v] methionine supplemented diet), respectively. We used Agilent Technologies miRNA microarray to examine microRNA expression in the liver and serum.
2024-01-31 | GSE252035 | GEO
Project description:Nonalcoholic fatty liver disease (NAFLD) is a hepatic condition characterized by excessive fat accumulation, leading to liver fibrosis, cirrhosis, and cancer. Currently, invasive liver biopsy is the only method for identifying and classifying NASH. Mass spectrometry-based proteomics can detect crucial proteins and pathways involved in NASH development. A study using liver and serum samples from mice and humans found altered proteins involved in detoxification, fibrosis, inflammation, and fatty acid metabolism. These findings provide insights into NASH molecular mechanisms and potential diagnostic biomarkers for early diagnosis.
2025-05-07 | PXD053187 | Pride
Project description:Exosomal or serum miRNA in liver disease
| PRJNA339060 | ENA
Project description:Human genetic studies have identified several MARC1 variants as protective against non-alcoholic fatty liver diseases (NAFLD). The MARC1 variants are associated with reduced lipid profiles, liver enzymes, and liver-related mortality. However, the role of mitochondrial amidoxime reducing component 1 (mARC1), encoded by MARC1, in NAFLD is still unknown and the therapeutic potential of this target has never been developed. Given that mARC1 is mainly expressed in hepatocytes, we developed an N-acetylgalactosamine conjugated mouse mARC1 siRNA to address this. In ob/ob mice, knockdown of mARC1 in mouse hepatocytes resulted in decreased liver weight, serum lipid enzymes, low-density lipoprotein cholesterol, and liver triglycerides. Loss of mARC1 also improved the lipid profiles and attenuated liver pathological changes in two diet-induced nonalcoholic steatohepatitis (NASH) mouse models. A comprehensive analysis of mARC1-deficient liver in NASH by metabolomics, proteomics, and lipidomics showed that mARC1 knockdown partially restored metabolites and lipids altered by diets. Taken together, loss of mARC1 protects mouse liver from NASH, suggesting a potential therapeutic approach of NASH by downregulation of mARC1 in hepatocytes.
2023-04-28 | MSV000091820 | MassIVE
Project description:To identify miRNAs that play important roles in the liver carcinogenesis from NASH, miRNA expression profiles were examined. Some miRNAs showed aberrant expression in HCC (Hepatocellular carcinoma) from NASH (non-alcoholic steatohepatitis). These miRNAs were regulated by DNA methylation, and could be potential therapeutic targets for HCC (Hepatocellular carcinoma) from NASH (non-alcoholic steatohepatitis).
2014-12-01 | GSE52821 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is characterized by a series of pathological changes that can progress from simple fatty liver disease to non-alcoholic steatohepatitis (NASH). The objective of this study is to describe changes in global gene expression associated with the progression of NAFLD. This study is focused on the expression levels of genes responsible for the absorption, distribution, metabolism and excretion (ADME) of drugs. Differential gene expression between three clinically defined pathological groups; normal, steatosis and NASH was analyzed. The samples were diagnosed as normal, steatotic, NASH with fatty liver (NASH fatty) and NASH without fatty liver (NASH NF). Genome-wide mRNA levels in samples of human liver tissue were assayed with Affymetrix GeneChipM-. Human 1.0ST arrays
2011-07-12 | E-MEXP-3291 | biostudies-arrayexpress
Project description:miRNAs have been found to circulate in the blood in a cell-free form; their potential as readily accessible disease markers is currently evaluated. Here, we investigated if miRNA expression profile in peripheral blood can be useful as disease parameter in patients with chronic hepatitis C (CHC), chronic hepatitis B (CHB), non-alcoholic steatohepatitis (NASH), and normal liver (NL). RNA from exosome rich fraction was extracted from serum of patients with 64 CHC, 4 CHB, 7 NASH, and 12 healthy volunteers. miRNA expression profile was analyzed by microarray. Histological evaluation for the degree of inflammation and fibrosis in liver disease patients was also performed. miRNA expression profile according to the degree of liver fibrosis and inflammation was established. Diagnosis of fibrosis, inflammation by using miRNA expression pattern was shown with accuracy 67.2~89.1%, 67.2~76.5%, respectively. Moreover, miRNA expression profile in several liver diseases was also established. Classification among CHC, CHB, NASH, and NL was well tolerated and reproducible. The expression pattern of miRNA in peripheral blood showed not only the useful parameter of the grade and stage of liver disease, but also diagnostic tool for liver disease.
2012-11-05 | GSE33857 | GEO
Project description:MicroRNAs (miRNAs) have emerged as potential therapeutic targets for non-alcoholic fatty liver disease/non-alcoholic steatohepatitis (NAFLD/NASH). Traditional Chineses Medicine (TCM) plays an important role in the prevention or treatment of NAFLD/NASH. However, miRNA targets of TCM against NASH still remain largely unknown. Here, we showed that Yiqi-Bushen-Tiaozhi (YBT) recipe effectively attenuated diet-induced NASH in C57BL/6 mice. To identify the miRNA targets of YBT and understand the potential underlying mechanisms, we performed network pharmacology using miRNA and mRNA deep sequencing data combined with Ingenuity Pathway Analysis (IPA). Mmu-let-7a-5p, mmu-let-7b-5p, mmu-let-7g-3p and mmu-miR-106b-3p were screened as the main targets of YBT. Our results suggested that YBT might alleviate NASH by regulating the expression of these miRNAs that potentially modulate inflammation/immunity and oxidative stress. This study provides useful information for guiding future studies on the mechanism of YBT against NASH by regulating miRNAs.
2020-12-07 | GSE144721 | GEO
Project description:Nonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress-induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. Here we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA-seq and ChIP-seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte-specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated the molecular signature of NASH and sensitized mice to diet-induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB that promotes inflammatory signaling in hepatocytes and stress-induced cell death. These findings illustrate a novel mechanism through which disruptions of chromatin architecture drive the emergence of disease-specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.
2019-09-10 | GSE131336 | GEO
Project description:Non-alcoholic fatty liver disease (NAFLD) is a predominant form of chronic liver disease, affecting nearly 25 % of the global population. The progression from steatosis to nonalcoholic steatohepatitis (NASH) in NAFLD patients is one of the major causes of liver-related death worldwide. We assessed the miRNA expression profiles of the exosomes derived from the peripheral blood of NASH patients or healthy controls.
2022-06-01 | GSE202167 | GEO