Liver disease

Liver disease, or hepatic disease, is any of many diseases of the liver. If long-lasting it is termed chronic liver disease. Although the diseases differ in detail, liver diseases often have features in common. Liver diseases File:Ground glass hepatocytes high mag cropped 2.jpg|Ground glass hepatocytes File:Primary biliary cirrhosis intermed mag much cropping.jpg|Primary biliary cirrhosis File:Buddchiari2.PNG|Budd-chiari syndrome File:Non-alcoholic_fatty_liver_disease1.jpg| [[Micrograph]] of [[non-alcoholic fatty liver disease]] There are more than a hundred different liver diseases. Some of the most common are:

Fascioliasis, a parasitic infection of liver caused by a liver fluke of the genus Fasciola, mostly Fasciola hepatica.
Hepatitis, inflammation of the liver, is caused by various viruses (viral hepatitis) also by some liver toxins (e.g. alcoholic hepatitis), autoimmunity (autoimmune hepatitis) or hereditary conditions.
Alcoholic liver disease is a hepatic manif

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A Human Liver-on-a-Chip Platform for Modeling Nonalcoholic Fatty Liver Disease

Soufian Lasli

The liver possesses a unique microenvironment with a complex internal vascular system and cell-cell interactions. Nonalcoholic fatty liver disease (NAFLD) is the most common form of chronic liver disease, and although much effort has been dedicated to building models to target NAFLD, most in vitro systems rely on simple models failing to recapitulate complex liver functions. Here, an in vitro system is presented to study NAFLD (steatosis) by coculturing human hepatocellular carcinoma (HepG2) cells and umbilical vein endothelial cells (HUVECs) into spheroids. Analysis of colocalization of HepG2-HUVECs along with the level of steatosis reveals that the NAFLD pathogenesis could be better modeled when 20% of HUVECs are presented in HepG2 spheroids. Spheroids with fat supplements progressed to the steatosis stage on day 2, which could be maintained for more than a week without being harmful for cells. Transferring spheroids onto a chip system with an array of interconnected hexagonal microwells proves helpful for monitoring functionality through increased albumin secretions with HepG2-HUVEC interactions and elevated production of reactive oxygen species for steatotic spheroids. The reversibility of steatosis is demonstrated by simply stopping fat-based diet or by antisteatotic drug administration, the latter showing a faster return of intracellular lipid levels to the basal level.

2019

Differentiation of human embryonic stem cells to hepatocytes

Noam Beckmann

Many liver diseases involve hepatocyte malfunction. In most cases, transplantation of corrected hepatocytes would correct for disease symptoms. Liver donor shortage and hepatocyte inability to proliferate in vitro accentuate this problem. Embryonic stem and induced pluripotent stem cells proliferate indefinitely and have the capacity to differentiate into every cell type of the body. They could thus represent a solution to this organ donor shortage. In this project, we aim to differentiate ES and iPS cells to hepatocytes. First, we consider an approach to select the ES/iPS cell line showing the best potential to generate liver lineage using teratomas as a selection tool. Then we use lentiviral vectors to transduce this selected cell line with essential liver-‐specific development factors to help differentiation efficiency. Next, we developed an in vitro differentiation protocol based on existing protocols and developmental clues of liver development to generate a pool of hepatocyte precursors. Later on, we injected these differentiated cells in mice liver of Fah-‐, Rag2-‐ and Il-‐2rγ-‐deficient mice to check for engraftment and liver marker expression. Our findings show, after checking for hepatocyte-‐ specific markers in the differentiated cells, that our previous selection for the potentially best cell line seems correct. We also find that the transcription factors involved in liver development appear to have a negative effect in vitro on liver differentiation. Applying our protocol to regular ES cells results on the production of late maturity hepatocyte markers, showing correct differentiation and maturation of newly formed hepatocytes. Finally, mouse in vivo liver transplantation of these differentiated cells gives us human albumin expression detectable in blood serum of said mice

2010

In Vitro Human Liver Model of Nonalcoholic Steatohepatitis by Coculturing Hepatocytes, Endothelial Cells, and Kupffer Cells

Soufian Lasli

The liver has a complex and unique microenvironment with multiple cell-cell interactions and internal vascular networks. Although nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease with multiple phases, no proper model could fully recapitulate the in vivo microenvironment to understand NAFLD progression. Here, an in vitro human liver model of NAFLD by coculturing human hepatocytes, umbilical vein endothelial cells (HUVECs), and Kupffer cells (KCs) into spheroids is presented. Analysis of indirect cross-talk using conditioned media between steatotic spheroids-composed of hepatocellular carcinoma-derived cells (HepG2) and HUVECs-and mouse KCs reveals that the latter can be activated showing increased cell area, elevated production of reactive oxygen species (ROS), and proinflammatory cytokines. Spheroids incorporating human KCs (HKCs) can also be induced into steatotic stage by supplementing fat. Steatotic spheroids with/without HKCs show different levels of steatotic stages through lipid accumulation and ROS production. Steatotic spheroids made from an immortalized hepatic progenitor cell line (HepaRG) compared to those made from HepG2 cells display similar trends of functionality, but elevated levels of proinflammatory cytokines, and improved reversibility of steatosis. The in vitro human liver system proposed makes strides in developing a model to mimic and monitor the progression of NAFLD.

2019

Cirrhosis

Cirrhosis, also known as liver cirrhosis or hepatic cirrhosis, and end-stage liver disease, is the impaired liver function caused by the formation of scar tissue known as fibrosis due to damage cause

Hepatitis

Hepatitis is inflammation of the liver tissue. Some people or animals with hepatitis have no symptoms, whereas others develop yellow discoloration of the skin and whites of the eyes (jaundice), poor a

Non-alcoholic fatty liver disease

Metabolic (dysfunction) associated fatty liver disease (MAFLD) was previously known as non-alcoholic fatty liver disease (NAFLD) until renamed in 2023 by a global consensus panel composed mostly of h

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