Hepatocyte Regeneration
Hepatocyte Regeneration - Related Videos
08:14
Hepatocyte-specific Ablation in Zebrafish to Study Biliary-driven Liver Regeneration
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Cited by 18 •
2015
To help assess the molecular mechanisms underlying zebrafish biliary-driven liver regeneration, we established a liver injury model in which the nitroreductase-expressing hepatocytes are genetically ablated upon metronidazole treatment. In this protocol, we describe how to adeptly manipulate, monitor and analyze hepatocyte ablation and biliary-driven liver regeneration.
10:42
Development of an Ethanol-induced Fibrotic Liver Model in Zebrafish to Study Progenitor Cell-mediated Hepatocyte Regeneration
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Cited by 7 •
2016
Sustained fibrosis with deposition of excessive extracellular matrix proteins leads to cirrhosis. Alcohol abuse is one of the main causes of severe liver disease. We established an ethanol-induced zebrafish fibrotic liver model to study the mechanisms and strategies of promoting hepatocyte regeneration upon alcohol-induced injury.
10:04
Isolation of Regenerating Hepatocytes after Partial Hepatectomy in Mice
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2022
Lipid-laden hepatocytes are inherent to liver regeneration but are usually lost upon density-gradient centrifugation. Here, we present an optimized cell isolation protocol that retains steatotic hepatocytes, yielding representative populations of regenerating hepatocytes after partial hepatectomy in mice.
11:24
Intrasplenic Transplantation of Hepatocytes After Partial Hepatectomy in NOD.SCID Mice
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Cited by 1 •
2018
We have described a protocol for performing partial hepatectomy (PHx) and cell transplantation via spleen in NOD.SCID (NOD.CB17-Prkdcscid/J) mice. In this protocol, an incision is made to expose and resect the left lobe of the liver followed by another incision for the intrasplenic transplantation of cells.
03:39
Targeted Liver Ablation: Inducing Hepatocyte Death with Metronidazole in Transgenic Zebrafish Larvae
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2023
The article describes targeted liver ablation, a method for inducing hepatocyte death with metronidazole in transgenic zebrafish larvae. The sample protocol describes the process for generating, manipulating and assessing targeted liver ablation in zebrafish.
FAQs
Cytokines and growth factors act as signals that encourage surviving hepatocytes to re-enter the cell cycle. The cells then replicate their DNA and divide, increasing the population available to restore lost tissue. This signaling response links the extent of injury with a coordinated proliferative reaction, helping explain how liver mass and function can recover after damage.
Nonparenchymal cells provide an important local context for hepatocyte responses. Their interactions with liver parenchymal cells help coordinate signals that regulate cell-cycle re-entry, proliferation, and restoration of tissue organization. Considering these cellular relationships prevents regeneration from being viewed as an isolated hepatocyte behavior and highlights how the tissue environment influences repair.
When hepatocyte proliferation is limited, progenitor or ductular cells may contribute to tissue restoration. This alternative response makes regeneration a question of cell-fate flexibility as well as cell division. Studying when this contribution occurs can reveal how the liver maintains repair capacity under conditions in which its primary parenchymal cells do not provide sufficient proliferation.
Hepatocyte regeneration demonstrates that mature liver cells can alter their behavior in response to tissue loss, rather than remaining permanently inactive. In developmental biology, this provides a model for examining how cell fate, organ size, and tissue architecture are coordinated during repair. The process therefore connects mechanisms of adult recovery with broader principles of developmental regulation.
A useful investigation can follow the coordinated response of surviving hepatocytes, including cell-cycle re-entry, DNA replication, and division after injury or partial tissue loss. It can also consider cytokine and growth-factor signals, interactions with nonparenchymal cells, and possible progenitor or ductular participation. These observations help relate cellular behavior to restored tissue mass and liver function.
The process is especially relevant when researchers examine how the liver responds to injury or partial loss of tissue. It offers a framework for connecting cellular proliferation with recovery of tissue mass and function. Because the response can involve mature hepatocytes and, when needed, progenitor or ductular cells, it also supports research on liver disease.
Findings from this field can identify how cytokines, growth factors, cellular interactions, and alternative progenitor responses coordinate liver repair. That information may guide research on therapies intended to support functional recovery rather than focusing only on cell replacement. The developmental-biology context is valuable because it links therapeutic strategies with regulation of cell fate, organ size, and tissue architecture.