ICAN BioCell – Human Liver BiologyOur research platform on chronic liver diseasesChronic liver disease is a major public health issue today, and a leading cause of death worldwide.
The ICAN BioCell Human Liver Biology Platform aims to produce primary human liver cells (hepatocytes and all non-parenchymal cells) and develop primary cultured liver models in 2D or 3D (thin slices or spheroids) to study chronic liver diseases, in particular fibrosis and NASH.
Our platform is accessible to all academic research units and open to industrial projects.DownloadYou are a patient?Thanks to a partnership between AP-HP, INSERM, Sorbonne Université and IHU ICAN, the ICAN BioCell Human Liver Biology platform combines technological innovation with the maintenance of a collection of human body samples and products.
Thank you to all the patients who agreed to take part in the ICAN BioCell Human Liver Biology collection! Research into chronic liver disease advances thanks to you. If you have made a donation to the Human HepCell collection and wish to object to one or more of the research projects, please contact the surgeon who operated on you, or let us know at protection.donnees.dsi@aphp.fr.More information
Our catalog
BioCell Human Liver Biology offers a catalog for the production and sale of different liver cell types:
- Fresh human hepatocytes (HH)
- Human liver myofibroblasts (HLMF) from normal liver, NASH, fibrosis and cirrhosis
- Non-parenchymal cells (NPCs)
- Endothelial cells, kupffer cells, immune cells…
- Bile cells from the gallbladder
- Precision cut liver slices (PCLS), healthy or pathological (NASH, fibrosis, cirrhosis). See scientific publication.
PCLS in primary cultivationIHC section of a PCLS
- Hepatic spheroid/organoid model See the scientific publication.
Our services
ICAN BioCell – Human Liver Biology also offers various services for research:
- Fibrosis: we evaluated the sensitivity of hepatic myofibroblasts from different patients (normal and cirrhotic) to antifibrotic molecules using our Quanti-Fibrosis® platform. Our data established differential efficacy of these molecules revealing the impact of human polymorphism and disease background on drug susceptibility.
- MASH: we have 2D and 3D models to study hepatic steatosis, whether or not associated with inflammation
- Hepatocytes (HH) or PCLS from fatty livers
- In vitro steatosis induction on normal HH or PCLS with fatty acids
MyofibroblastsNormal hepatocytesFatty hepatocytes (lipids in red)Untreated* steatotic PCLS*Immunolabeling of lipids in green and nuclei in blueSteatotic PCLS + degreasing cocktail*
- Lipid metabolism (dosage of triglycerides, RedOil staining, genes involved in lipid metabolism (beta Oxidation, export of lipids, autophagy, lipogenesis, etc.)
- Hepatic functional metabolism (albumin, CYP3A4 activity, ABC transporters…)
- Viability and toxicity (MTT, ATP and HDL) and oxidative stress (ROS detection), pro-inflammatory cytokines (QPCR and ELISA)
ContactLynda Aoudjehane (PhD)Project manager platform managerl.aoudjehane@ihuican.orgICAN BioCell Human Liver Biology
Faculté de Médecine de Sorbonne Université
Hôpital de la Pitié-Salpêtrière
91 boulevard de l’Hôpital
75013 ParisDownload the brochureScientific publicationsFocus on 2 major publications29/04/2020Novel defatting strategies reduce lipid accumulation in primary human culture models of liver steatosisToday, liver transplantation (HT) is the accepted treatment for end-stage chronic liver disease. There is currently a shortage of organs, and “marginal” grafts, in particular steatotic (fatty liver) grafts, are increasingly used to try and limit this shortage. Steatosis is the main reason why TH teams refuse liver transplants, as it is responsible for liver dysfunction after transplantation.
The use of steatotic grafts could alleviate some of the graft shortage currently affecting TH patients. Our strategy is to treat these “candidate” grafts prior to implantation, using normo-thermal perfusion (physiological temperature 37°C) to improve tolerance to ischemia and extract lipid vacuoles from hepatocytes.
Our “degreasing” method consists in acting directly on the excessive accumulation of lipids. In this study, we devised a “degreasing” cocktail designed to draw out the lipids stored in steatotic hepatocytes. To achieve this, we created a cocktail of molecules designed to activate each step in the metabolism of intra-hepatocyte lipids until they leave the cell.21/11/2019 Inhibition of receptor-interacting protein kinase-1 improves experimental non-alcoholic fatty liver diseaseHepatic steatosis is the accumulation of fats in the liver. Steatosis is very common (25% of the French population is affected) and is very often associated with overweight and type 2 diabetes. Often asymptomatic and of no consequence, fat accumulation is responsible in 30% of cases for inflammatory lesions of the liver (non-alcoholic steatohepatitis or NASH), which can lead to non-alcoholic cirrhosis and liver cancer.
The inflammation and death of liver cells in NASH is initially compensated for by the liver’s regenerative capacity. However, in the context of chronic liver damage, as observed in NASH, these healing capacities are deleterious and contribute to liver destruction (fibrosis). One of our current research objectives is to identify the mechanisms behind inflammation and cell death in NASH, in order to propose effective treatments.
Recently, our team demonstrated through work in mice and human liver cells that blocking cell death in NASH reduces abnormal liver inflammation and scarring, and limits fat accumulation in the liver.All platform publications06/02/2024Immunofluorescent Staining of Human Hepatic Multicellular Spheroids: A Model for Studying Liver Diseases07/2023Therapeutic potentials of mesenchymal stromal cells-derived extracellular vesicles in liver failure and marginal liver graft rehabilitation: a scoping review21/06/2023An Efficient 5-Aminolevulinic Acid Photodynamic Therapy Treatment for Human Hepatocellular Carcinoma10/02/2022MRCK-Alpha and Its Effector Myosin II Regulatory Light Chain Bind ABCB4 and Regulate Its Membrane Expression18/03/2021Ex-Vivo Pharmacological Defatting of the Liver: A Review02/03/2020Cancer-associated fibroblasts in cholangiocarcinoma12/10/2020Bifunctional Therapeutic Peptides for Targeting Malignant B Cells and Hepatocytes: Proof of Concept in Chronic Lymphocytic Leukemia19/05/2020Cold-Atmospheric Plasma Induces Tumor Cell Death in Preclinical In Vivo and In Vitro Models of Human Cholangiocarcinoma28/10/2019Impact of hepatitis C virus and alcohol, alone and combined, on the unfolded protein response in primary human hepatocytes22/10/2019Hepatitis C Virus Improves Human Tregs Suppressive Function and Promotes Their Recruitment to the Liver11/08/2016Heregulin-1ß and HER3 in hepatocellular carcinoma: status and regulation by insulin07/03/2016Development of an in vitro model to test antifibrotic drugs on primary human liver myofibroblasts.27/07/2015Infection of Human Liver Myofibroblasts by Hepatitis C Virus: A Direct Mechanism of Liver Fibrosis in Hepatitis C25/10/2013Hepatic myofibroblasts promote the progression of human cholangiocarcinoma through activation of epidermal growth factor receptor30/04/2013Mitogenic insulin receptor-A is overexpressed in human hepatocellular carcinoma due to EGFR-mediated dysregulation of RNA splicing factors09/11/2012Corticosteroids do not reverse the inhibitory effect of cyclosporine on regulatory T-cell activity in contrast to mycophenolate mofetil10/03/2012Epidermal growth factor receptor and HER-3 restrict cell response to sorafenib in hepatocellular carcinoma cells
