Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The identification of putative circulating miRNA biomarkers of Thioacetamide-induced hepatotoxicity.

ABSTRACT: The Thioacetamide-treated rat was first identified as a model of hepatotoxicity by Gupta in 1956 and is now well-established, not least because the histopathogical output closely mimics that seen in humans with chronic liver disease. Acute treatment of rats with Thioacetamide causes pronounced necrosis and inflammation. Animals received intraperitoneal (ip) doses of vehicle-only (0.9% (v/v) saline) (n=3), or 100 mg/kg Thioacetamide (n=3) and were sacrificed after 24 hours. Blood was withdrawn via the descending vena cava and immediately transferred into potassium/EDTA tubes. Following centrifugation (16,100g, 4°C, 5 min) the plasma was collected and stored at -80°C. miRNA microarray profiling of RNA extracted from the plasma of rats treated with Thioacetamide revealed that a subset of miRNAs were differentially expressed following treatment. These miRNAs appeared to mediate pathways involved in hepatic fibrosis and stellate cell activation, suggesting that they might function as predictive biomarkers following compound-induced hepatotoxicity. The changes correlated well with increases in ALT levels, which are the current gold standard method for determining the extent of liver injury. Furthermore, it is hypothesised that particular aetiologies of liver damage might cause differing expression profiles of miRNAs, thus certain miRNAs could be implemented in a panel-type expression study to distinguish between different types of hepatic injury.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE55885 | GEO | 2014/03/14

SECONDARY ACCESSION(S): PRJNA241250

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

The identification of putative circulating miRNA biomarkers of Thioacetamide-induced hepatotoxicity.

Project description:The Thioacetamide-treated rat was first identified as a model of hepatotoxicity by Gupta in 1956 and is now well-established, not least because the histopathogical output closely mimics that seen in humans with chronic liver disease. Acute treatment of rats with Thioacetamide causes pronounced necrosis and inflammation. Animals received intraperitoneal (ip) doses of vehicle-only (0.9% (v/v) saline) (n=3), or 100 mg/kg Thioacetamide (n=3) and were sacrificed after 24 hours. Blood was withdrawn via the descending vena cava and immediately transferred into potassium/EDTA tubes. Following centrifugation (16,100g, 4M-BM-0C, 5 min) the plasma was collected and stored at -80M-BM-0C. miRNA microarray profiling of RNA extracted from the plasma of rats treated with Thioacetamide revealed that a subset of miRNAs were differentially expressed following treatment. These miRNAs appeared to mediate pathways involved in hepatic fibrosis and stellate cell activation, suggesting that they might function as predictive biomarkers following compound-induced hepatotoxicity. The changes correlated well with increases in ALT levels, which are the current gold standard method for determining the extent of liver injury. Furthermore, it is hypothesised that particular aetiologies of liver damage might cause differing expression profiles of miRNAs, thus certain miRNAs could be implemented in a panel-type expression study to distinguish between different types of hepatic injury. Single channel miRNA microarrays were performed on n= 3 samples, 2 treatment groups; control and test. Control animals received vehicle-only (0.9% (v/v) saline) via the ip route. Test animals received 100 mg/kg Thioacetamide dissolved in 0.9% (v/v) saline, via the ip route. 24 h after dosing animals were sacrificed using decapitation under terminal anaesthesia.

2014-03-14 | E-GEOD-55885 | biostudies-arrayexpress

A time-course study of thioacetamide (TAA)-induced liver fibrosis in rats

Project description:The aim is to characterize rat liver fibrosis induced by thioacetamide (TAA). To induce hepatic fibrosis, Male Sprague Dawley rats (9-12 weeks of age and 380-420 g of weight upon arrival, supplied by Beijing Vital River laboratory animal Co., Ltd.) were treated with thioacetamide (TAA). Rat liver samples were collected from five groups of rats at week 1, 2, 4, 8 and 13 after TAA (300 mg/kg) administration three times per week while five control groups receive the same volume of 0.9% normal saline. Four biological replicates were used for each group.

2021-09-29 | E-MTAB-10547 | biostudies-arrayexpress

Identification of microRNAs with the potential role in progression of thioacetamide-induced liver fibrosis in mouse

Project description:We applied Solexa deep sequencing technology to identify which miRNAs were regulated in thioacetamide-induced fibrotic liver tissue

2016-04-15 | GSE79865 | GEO

In vivo transcriptomic responses to thioacetamide exposure in rat liver, kidney, and heart tissue

Project description:In this study we tested the ability to predict organ injury from transcriptomics data in Sprague-Dawley rats at early time points after exposure to thioacetmide (8 and 24 hours). We selected thioacetamide, an organosulfur compound extensively used in animal studies as a hepatotoxin and carcinogen for its ability to cause acute liver damage.

2018-09-20 | GSE120195 | GEO

Probing liver injury induced by thioacetamide in human in vitro pooled hepatocyte experiments

Project description:In this study we tested the ability to predict liver injury from in vitro human pooled hepatocyte data after exposure to thioacetamide (24 hour). We selected thioacetamide, a compound extensively used in various studies for its ability to cause liver injury.

2024-04-03 | GSE250139 | GEO

In the livers of rats treated with thioacetamide for 28 days

Project description:To clarify the regulatory molecular mechanisms behind cell cycle aberrations related to the early stages of hepatocarcinogenesis. We investigated the early stage of hepatocarcinogenesis using global expression analyses. Livers from rats treated with thioacetamide were subjected to microarray analysis. Results were compared with livers from rats untreated controls (n = 4 animals/group).

2012-12-21 | E-GEOD-43066 | biostudies-arrayexpress

In vivo transcriptomic responses to thioacetamide exposure in guinea pig liver tissue

Project description:In this study we tested the ability to predict organ injury from transcriptomic data in Hartley guinea pigs at early time points after exposure to thioacetamide (9 and 33 hours). We selected thioacetamide, a compound extensively used in animal studies for its ability to cause liver damage.

2021-03-25 | GSE169545 | GEO

In vitro transcriptomic responses to thioacetamide-S-oxide exposure in human primary hepatocytes, renal tube epithelial, and cardiomyocytes

Project description:In this study we tested the ability to predict organ injury endpoints from in vitro transcriptomics responses at early time points (9 and 24 hours) after to thioacetamide-S-oxide treatment, the toxic metabolite of thioacetamide. Thioacetamide, an organosulfur compound, have been extensively used in animal studies as a hepatotoxin and carcinogen for its ability to cause acute liver damage.

2020-06-03 | GSE134641 | GEO

Mechanistic roles of microRNAs in hepatocarcinogenesis: A study of thioacetamide with multiple doses and time-points of rats

Project description:Environmental chemicals exposure are one of the primary factors for liver toxicity and hepatocarcinoma. Thioacetamide (TAA) is a well-known hepatotoxicant and could be a liver carcinogen in humans.The discovery of early and sensitive biomarkers in liver injury and tumor progression could improve cancer diagnosis, prognosis, and management. In the present study, we studied the dynamic changes in microRNAs (miRNAs) expression and explored the potential mechanistic role of miRNAs in rat liver treated with TAA at multiple doses and time points. Sprague-Dawley rats were administrated with TAA at three doses [low (4.5 mg/kg), middle (15mg/kg) and high (45mg/kg)] and four repeated treatment durations (3-, 7-, 14- and 28-days). Expressions of miRNAs in livers were profiled using next generation sequencing and analyzed. Overall, 330 unique differentially expressed miRNAs (DEMs) were identified in the entire TAA-treatment course. Of these, 129 DEMs were found significantly enriched for the “liver cancer” annotation. These results were further complemented by pathway analysis in which “Molecular Mechanisms of Cancer”, “p53-”, “TGF-β-”, “MAPK-” and “Wnt-signaling” were significantly enriched in most TAA-treatment conditions. Two miRNAs (rno-miR-34a-5p and rno-miR-455-3p) out of 48 DEMs (common across all the treatment conditions) were identified to be early and sensitive biomarkers for TAA-induced hepatocarcinogenicity. Upregulation of rno-miR-34a-5p was further confirmed by qPCR. These findings reveal the critical role of miRNAs in the mechanisms underlying hepatocarcinogenesis and potential application for human risk assessment. Most importantly, rno-miR-34a-5p is the most suitable early and sensitive biomarker for TAA-induced hepatocarcinogenesis due to its consistent elevation during the entire treatment course.

2017-06-23 | GSE87446 | GEO

In vitro transcriptomic responses to thioacetamide-S-oxide exposure in Sprague-Dawley rat primary hepatocytes, renal tube epithelial, and cardiomyocytes

2019-11-19 | GSE134569 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data