Efficacy of primary liver organoid culture from different stages of non-alcoholic steatohepatitis (NASH) mouse model

Elbadawy, Mohamed; Yamanaka, Megumi; Goto, Yuta; Hayashi, Kimika; Tsunedomi, Ryouichi; Hazama, Shoichi; Nagano, Hiroaki; Yoshida, Toshinori; Shibutani, Makoto; Ichikawa, Ryo; Nakahara, Jin; Omatsu, Tsutomu; Mizutani, Tetsuya; Katayama, Yukie; Shinohara, Yuta; Abugomaa, Amira; Kaneda, Masahiro; Yamawaki, Hideyuki; Usui, Tatsuya; Sasaki, Kenji

doi:10.1016/j.biomaterials.2020.119823

Cited by 66 publications

(56 citation statements)

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“…Multicellular interactions in NASH, although critical to pathogenesis, have been difficult to model. Substantial progress in generating organoid models derived from pluripotent stem cells (Collin de l'Hortet et al, 2019;Ouchi et al, 2019;Ramli et al, 2020) primary liver organoids (Elbadawy et al, 2020), microtissues (Feaver et al, 2016;Vacca et al, 2020), or spheroids using cell lines (Pingitore et al, 2019) offers the prospect of dissecting these interactions and establishing a platform for highthroughput testing of candidate therapeutic agents.…”

Section: Role Of the Gut Microbiota In Development Of Nafld And Nashmentioning

confidence: 99%

Mechanisms and disease consequences of nonalcoholic fatty liver disease

Loomba

Friedman

Shulman³

2021

Cell

1,118

778

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Section: Role Of the Gut Microbiota In Development Of Nafld And Nashmentioning

confidence: 99%

Mechanisms and disease consequences of nonalcoholic fatty liver disease

Loomba

Friedman

Shulman³

2021

Cell

1,118

778

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“…Simplicity of operator, commonly used, high reproducibility Highly toxic Müller et al, 1988;Fontana et al, 1996;Wei et al, 2014;Wallace et al, 2015;Inoue et al, 2018 -Garay et al, 1996;Kirkland et al, 2010;Heinrich et al, 2011;Tag et al, 2015 Kanzler et al, 1999;Ueberham et al, 2003;Thieringer et al, 2008;Fransén-Pettersson et al, 2016;Nishio et al, 2019;Yoshiji et al, 2000 Leite et al, 2016;Artegiani and Clevers, 2018;Coll et al, 2018;Ouchi et al, 2019;Pingitore et al, 2019;Prior et al, 2019;Brovold et al, 2020;Chusilp et al, 2020;Elbadawy et al, 2020 Frontiers in Physiology | www.frontiersin.org FIGURE 2 | Organoid models of liver fibrosis. The generation of liver organoids and liver fibrosis models.…”

Section: Intraperitoneal Injectionmentioning

confidence: 99%

“…Liver organoids were generated from mice with mild (NASH A), moderate (NASH B), and severe (NASH C) methionine and choline deficiency diets-induced NASH models that reproduce the characteristics of NASH disease liver tissue. The NASH liver organoid model can be used to study genetic stability and/or lipid metabolism during NAFLD/NASH transformation ( Elbadawy et al, 2020 ).…”

Section: Organoid Liver Fibrosis Modesmentioning

confidence: 99%

Animal and Organoid Models of Liver Fibrosis

et al. 2021

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Liver fibrosis refers to the process underlying the development of chronic liver diseases, wherein liver cells are repeatedly destroyed and regenerated, which leads to an excessive deposition and abnormal distribution of the extracellular matrix such as collagen, glycoprotein and proteoglycan in the liver. Liver fibrosis thus constitutes the pathological repair response of the liver to chronic injury. Hepatic fibrosis is a key step in the progression of chronic liver disease to cirrhosis and an important factor affecting the prognosis of chronic liver disease. Further development of liver fibrosis may lead to structural disorders of the liver, nodular regeneration of hepatocytes and the formation of cirrhosis. Hepatic fibrosis is histologically reversible if treated aggressively during this period, but when fibrosis progresses to the stage of cirrhosis, reversal is very difficult, resulting in a poor prognosis. There are many causes of liver fibrosis, including liver injury caused by drugs, viral hepatitis, alcoholic liver, fatty liver and autoimmune disease. The mechanism underlying hepatic fibrosis differs among etiologies. The establishment of an appropriate animal model of liver fibrosis is not only an important basis for the in-depth study of the pathogenesis of liver fibrosis but also an important means for clinical experts to select drugs for the prevention and treatment of liver fibrosis. The present study focused on the modeling methods and fibrosis characteristics of different animal models of liver fibrosis, such as a chemical-induced liver fibrosis model, autoimmune liver fibrosis model, cholestatic liver fibrosis model, alcoholic liver fibrosis model and non-alcoholic liver fibrosis model. In addition, we also summarize the research and application prospects concerning new organoids in liver fibrosis models proposed in recent years. A suitable animal model of liver fibrosis and organoid fibrosis model that closely resemble the physiological state of the human body will provide bases for the in-depth study of the pathogenesis of liver fibrosis and the development of therapeutic drugs.

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“…Primary liver organoids according to the severity of NASH have also been successfully generated from mice. These different NASH organoids also display the upregulation of TNFa and IL1b at the early stage of NASH, for example (149). Pre-clinical studies and some clinical trials demonstrate promising results but also underline the complex nature of these chronic liver diseases.…”

Section: Resultsmentioning

confidence: 96%

Chronic Inflammation in Non-Alcoholic Steatohepatitis: Molecular Mechanisms and Therapeutic Strategies

et al. 2020

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Non-Alcoholic Steatohepatitis (NASH) is the progressive form of Non-Alcoholic Fatty Liver Disease (NAFLD), the main cause of chronic liver complications. The development of NASH is the consequence of aberrant activation of hepatic conventional immune, parenchymal, and endothelial cells in response to inflammatory mediators from the liver, adipose tissue, and gut. Hepatocytes, Kupffer cells and liver sinusoidal endothelial cells contribute to the significant accumulation of bone-marrow derived-macrophages and neutrophils in the liver, a hallmark of NASH. The aberrant activation of these immune cells elicits harmful inflammation and liver injury, leading to NASH progression. In this review, we highlight the processes triggering the recruitment and/or activation of hepatic innate immune cells, with a focus on macrophages, neutrophils, and innate lymphoid cells as well as the contribution of hepatocytes and endothelial cells in driving liver inflammation/fibrosis. On-going studies and preliminary results from global and specific therapeutic strategies to manage this NASH-related inflammation will also be discussed.

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Efficacy of primary liver organoid culture from different stages of non-alcoholic steatohepatitis (NASH) mouse model

Cited by 66 publications

References 50 publications

Mechanisms and disease consequences of nonalcoholic fatty liver disease

Mechanisms and disease consequences of nonalcoholic fatty liver disease

Animal and Organoid Models of Liver Fibrosis

Chronic Inflammation in Non-Alcoholic Steatohepatitis: Molecular Mechanisms and Therapeutic Strategies

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