deLiver'in Regeneration: Injury Response and Development

Curado, Silvia; Stainier, Didier Y. R.

doi:10.1055/s-0030-1255357

Cited by 14 publications

(19 citation statements)

References 82 publications

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Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

“…One of the oldest and most commonly used rodent models of liver regeneration is partial hepatectomy (PH), in which two-thirds of the animal's liver is surgically removed (74,75). Liver regeneration following PH is mainly driven by replication of existing hepatocytes and occurs in the absence of substantial necrosis and inflammation (74). To model how the liver regenerates when the ability of hepatocytes to divide is compromised, hepatocyte proliferation inhibitors such as 2-acetylaminofluorene can be administered before PH (2AAF/PH), which results in liver repopulation mediated by activation of liver progenitor cells or oval cells rather than proliferation of hepatocytes (74).…”

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

“…Liver regeneration following PH is mainly driven by replication of existing hepatocytes and occurs in the absence of substantial necrosis and inflammation (74). To model how the liver regenerates when the ability of hepatocytes to divide is compromised, hepatocyte proliferation inhibitors such as 2-acetylaminofluorene can be administered before PH (2AAF/PH), which results in liver repopulation mediated by activation of liver progenitor cells or oval cells rather than proliferation of hepatocytes (74). Other rodent models of liver injury and regeneration involve chemical treatments with carbon tetrachloride (CCl 4 ) or acetaminophen (reviewed in ref.…”

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

“…As with rodents, PH or toxic chemicals can be used to induce liver regeneration in zebrafish (reviewed in ref. 74). Genetic tools have enabled the development of additional regeneration models including the nitroreductase/ metronidazole cell ablation system (91) and morpholino-based knockdown of a mitochondrial import gene to induce hepatocyte death (92).…”

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

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Hepatic stellate cells in liver development, regeneration, and cancer

Yin¹,

Evason²,

Asahina³

et al. 2013

J. Clin. Invest.

595

567

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Hepatic stellate cells are liver-specific mesenchymal cells that play vital roles in liver physiology and fibrogenesis. They are located in the space of Disse and maintain close interactions with sinusoidal endothelial cells and hepatic epithelial cells. It is becoming increasingly clear that hepatic stellate cells have a profound impact on the differentiation, proliferation, and morphogenesis of other hepatic cell types during liver development and regeneration. In this Review, we summarize and evaluate the recent advances in our understanding of the formation and characteristics of hepatic stellate cells, as well as their function in liver development, regeneration, and cancer. We also discuss how improved knowledge of these processes offers new perspectives for the treatment of patients with liver diseases.

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Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

Section: Hepatic Stellate Cells In Liver Regenerationmentioning

confidence: 99%

See 2 more Smart Citations

Hepatic stellate cells in liver development, regeneration, and cancer

Yin¹,

Evason²,

Asahina³

et al. 2013

J. Clin. Invest.

595

567

View full text Add to dashboard Cite

show abstract

“…In experimental models, the liver was able to regenerate from partial hepatectomy (PHx) from 5 to 8 days in rodents. 3 Hepatocytes rarely proliferate in healthy adults but following 70% PHx, hepatocytes divide once or twice before returning to a quiescent state. 4 The ability of the liver to regenerate is a process which requires interplay between several pathways (cytokines, growth factors and metabolic networks).5 Changes in anyone of these pathways can impair the ability of the liver to regenerate from injury.…”

Section: Introductionmentioning

confidence: 99%

Acetaldehyde dehydrogenase 2 (ALDH2) activation protects hepatocytes from mitochondrial damage and death caused by 4-hydroxynonenal.

Baldauf¹

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Baldauf, Keegan J. 1982-, "Acetaldehyde dehydrogenase 2 (ALDH2) activation protects hepatocytes from mitochondrial damage and death caused by 4-hydroxynonenal." (2012 Alcoholic liver disease (ALD) ranks among the major causes of morbidity and mortality in the world and effects millions of patients each year. Progression of ALD is well characterized and is actually a spectrum of liver diseases, which progresses from steatosis, to inflammation and necrosis, to finally fibrosis and cirrhosis. However, the underlying mechanism(s) of ALD are not as well understood, and as a result there is no FDA-approved therapy to prevent or reverse the disease. With a better understanding of the mechanism(s) and risk factors that mediate the initiation and progression of ALD, a targeted therapy can be developed to treat or prevent it. The regenerative capacity of the liver is inhibited in fibrosis and cirrhosis. By enhancing the regenerative ability of the liver we may be able to reverse the effects of ALD. Indeed, recent in vivo studies by this group indicate that activating Aldehyde Dehydrogenase 2 (ALDH2) with Alda-1 (a novel ALDH2 activator) or Ethanol (EtOH) protects against oxidative stress and damage to the liver, as result enhancing regeneration. Because ALDH2 can protect mitochondria from oxidative stress that results from partial hepatectomy, oxidative stress from other sources should be protected against as well. To test this hypothesis, primary hepatocytes were isolated from mice and plated on 96-well plates for analysis via Cellomics High Content Screening. Some mice were administered EtOH for 3 days prior to hepatocyte isolation or exposed to Alda-1 to activate ALDH2. Cells were exposed to 4-Hydroxynonenal (4-HNE; 0-1000 j.JM) for 0-24 H. Activation of ALDH2, by pretreatment with EtOH or Alda-1 preexposure, clearly protected isolated hepatocytes from 4-HNE toxicity. Mitochondrial membrane potential was significantly increased in cells with IV activated ALDH2 and membrane permeability was decreased in these cells as well. These changes in hepatocyte viability indicate that activation of ALDH2 protects cells from oxidative stress.

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Zebrafish models to study hypoxia-induced pathological angiogenesis in malignant and nonmalignant diseases

Jensen¹,

Rouhi²,

Cao³

et al. 2011

Birth Defects Research Part C: Embryo Today: Reviews

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Most in vivo preclinical disease models are based on mouse and other mammalian systems. However, these rodent-based model systems have considerable limitations to recapitulate clinical situations in human patients. Zebrafish have been widely used to study embryonic development, behavior, tissue regeneration, and genetic defects. Additionally, zebrafish also provides an opportunity to screen chemical compounds that target a specific cell population for drug development. Owing to the availability of various genetically manipulated strains of zebrafish, immune privilege during early embryonic development, transparency of the embryos, and easy and precise setup of hypoxia equipment, we have developed several disease models in both embryonic and adult zebrafish, focusing on studying the role of angiogenesis in pathological settings. These zebrafish disease models are complementary to the existing mouse models, allowing us to study clinically relevant processes in cancer and nonmalignant diseases, which otherwise would be difficult to study in mice. For example, dissemination and invasion of single human or mouse tumor cells from the primary site in association with tumor angiogenesis can be studied under normoxia or hypoxia in zebrafish embryos. Hypoxia-induced retinopathy in the adult zebrafish recapitulates the clinical situation of retinopathy development in diabetic patients or age-related macular degeneration. These zebrafish disease models offer exciting opportunities to understand the mechanisms of disease development, progression, and development of more effective drugs for therapeutic intervention.

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deLiver'in Regeneration: Injury Response and Development

Cited by 14 publications

References 82 publications

Hepatic stellate cells in liver development, regeneration, and cancer

Hepatic stellate cells in liver development, regeneration, and cancer

Acetaldehyde dehydrogenase 2 (ALDH2) activation protects hepatocytes from mitochondrial damage and death caused by 4-hydroxynonenal.

Zebrafish models to study hypoxia-induced pathological angiogenesis in malignant and nonmalignant diseases

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