ArticleBasic & clinical pharmacology & toxicology2016
Bile Acid-Induced Toxicity in HepaRG Cells Recapitulates the Response in Primary Human Hepatocytes.
Article in Basic & clinical pharmacology & toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Lithocholic acid alleviates fatty liver in mice and non-human primate macaques.Life metabolism · 2026Article
- Cell-based approaches for the mechanistic understanding of drug-induced cholestatic liver injury.Archives of toxicology · 2025Review
- RIPK3 promoter hypermethylation in hepatocytes protects from bile acid-induced inflammation and necroptosis.Cell death & disease · 2023Article
- The assessment of the potential hepatotoxicity of new drugs byFrontiers in pharmacology · 2023Review
- Hepatotoxicity due to herbal dietary supplements: Past, present and the future.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2022Review
- Role of bile acids and their receptors in gastrointestinal and hepatic pathophysiology.Nature reviews. Gastroenterology & hepatology · 2022Review
- Fatty Acid Uptake in Liver Hepatocytes Induces Relocalization and Sequestration of Intracellular Copper.Frontiers in molecular biosciences · 2022Article
- Safety Evaluation of Porcine Bile Acids in Laying Hens: Effects on Laying Performance, Egg Quality, Blood Parameters, Organ Indexes, and Intestinal Development.Frontiers in veterinary science · 2022Article
- Assessment of long-term functional maintenance of primary human hepatocytes to predict drug-induced hepatoxicity in vitro.Archives of toxicology · 2021Article
- S100 calcium binding protein A6 and associated long noncoding ribonucleic acids as biomarkers in the diagnosis and staging of primary biliary cholangitis.World journal of gastroenterology · 2021Article
- Pyrrolizidine Alkaloids Disturb Bile Acid Homeostasis in the Human Hepatoma Cell Line HepaRG.Foods (Basel, Switzerland) · 2021Article
- Bile Acids as a New Type of Steroid Hormones Regulating Nonspecific Energy Expenditure of the Body (Review).Sovremennye tekhnologii v meditsine · 2021Review
- Prospect ofFrontiers in toxicology · 2021Review
- Differential toxic effects of bile acid mixtures in isolated mitochondria and physiologically relevant HepaRG cells.Toxicology in vitro : an international journal published in association with BIBRA · 2019Article
- Inflammation and Cell Death During Cholestasis: The Evolving Role of Bile Acids.Gene expression · 2019Review
- Animal models to study bile acid metabolism.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- In vitro prediction of drug-induced cholestatic liver injury: a challenge for the toxicologist.Archives of toxicology · 2018Article
- The impact of sterile inflammation in acute liver injury.Journal of clinical and translational research · 2017Article
- Microcystin-LR induced liver injury in mice and in primary human hepatocytes is caused by oncotic necrosis.Toxicon : official journal of the International Society on Toxinology · 2017Article
- Functional human induced hepatocytes (hiHeps) with bile acid synthesis and transport capacities: A novel in vitro cholestatic model.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cholestatic liver injury is a pathological component of numerous disease states. Much of the current literature on cholestatic liver injury is derived from in vitro studies using rodent hepatocytes or cell lines transfected with bile acid (BA) uptake transporters. While these studies demonstrate BA-driven apoptosis, it is debatable whether these models reflect the human pathophysiology, as primary human hepatocytes undergo primarily necrosis. HepaRG cells are a bipotential, human hepatoma line that express apical and basolateral BA transporters. Thus, we sought to determine whether HepaRG cells could replicate the response of primary human hepatocytes to BA exposure in vitro. HepG2 cells, primary murine hepatocytes (PMH) or HepaRG cells, were exposed to taurocholic acid (TCA), or glycochenodeoxycholate (GCDC) and lactate dehydrogenase release were measured to determine cell death. Cell death occurred dose-responsively in HepaRG cells when exposed to GCDC; however, HepG2 cells died acutely only at very high concentrations of GCDC. In HepaRG cells, pre-treatment with the caspase inhibitor z-VD-FMK had no effect on cell death, indicating a lack of apoptotic cell death, and while c-jun N-terminal kinase (JNK) protein was activated by GCDC treatment in HepaRG cells, the inhibition of JNK did not protect. Although previous data indicate that TCA stimulates pro-inflammatory gene induction in PMH, there was no change in gene expression after TCA stimulation in HepaRG cells, which mimicked previous data found in primary human hepatocytes. These data provide evidence for HepaRG cells as a new model for the study of the effect of BA on human hepatocytes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.