Hepatocyte Death
Hepatocyte Death - Related Videos
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.
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.
10:06
An Introduction to Cell Death
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2023
Necrosis, apoptosis, and autophagic cell death are all manners in which cells can die, and these mechanisms can be induced by different stimuli, such as cell injury, low nutrient levels, or signaling proteins. Whereas necrosis is considered to be an “accidental” or unexpected form of cell death, evidence exists that apoptosis and autophagy are both programmed and “planned” by cells.In this introductory video, JoVE highlights key discoveries pertaining to cell death, including recent work done...
12:11
Determination of Fatty Acid Oxidation and Lipogenesis in Mouse Primary Hepatocytes
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Cited by 39 •
2015
De novo lipogenesis and β-fatty acid oxidation constitute key metabolic pathways in hepatocyte, pathways that are perturbed in several metabolic disorders, including fatty liver disease. Here we demonstrate isolation of mouse primary hepatocytes and describe quantification of β-fatty acid oxidation and lipogenesis.
07:09
Isolation of Human Hepatocytes by a Two-step Collagenase Perfusion Procedure
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Cited by 93 •
2013
A modified two-step collagenase perfusion procedure for isolation of human hepatocytes is described. This method can also be applied to other mammalian livers. The isolated hepatocytes are available in high yield and viability, making them a suitable model for scientific research in areas such as liver regeneration, pharmacokinetics and toxicology.
FAQs
Apoptosis proceeds through caspase activation, a regulated enzymatic process that dismantles the cell in a controlled manner. This mechanism allows hepatocytes to be removed without the widespread membrane disruption associated with severe injury. In liver biology, recognizing caspase-associated cell dismantling helps investigators distinguish an orderly cellular response from damage that may provoke stronger inflammatory consequences.
Necrosis becomes biologically important because membrane disruption releases intracellular contents into surrounding tissue. Those released contents can promote inflammation, linking cell injury to changes beyond the individual hepatocyte. This distinction matters when interpreting liver damage: evidence of necrotic injury suggests a tissue response shaped not only by cell loss, but also by inflammatory effects associated with damaged cells.
Apoptosis and necrosis differ in both cellular control and tissue consequences. Caspase activation characterizes the controlled dismantling of apoptosis, whereas severe injury in necrosis disrupts membranes and releases intracellular contents. Comparing these features helps researchers interpret whether hepatocyte loss reflects a regulated biological process or uncontrolled damage, an important distinction in studies of disease, repair, and toxic exposure.
Hepatocyte death can arise from several biologically different stresses, including toxins, infections, metabolic disorders, and impaired blood flow. These causes are useful experimental categories because they connect the initiating condition with liver injury and repair. Comparing them allows investigators to ask whether a common pattern of cell loss appears across distinct insults or whether the context changes the resulting tissue response.
Researchers study hepatocyte death by measuring cell loss in experimental models of liver disease, regeneration, and chemical exposure. These measurements provide an observable way to evaluate how strongly an injury affects liver parenchymal cells and whether tissue responses accompany that loss. This approach supports disease modeling, investigation of repair, and assessment of potential harm from pharmaceuticals and other chemicals.
During liver regeneration studies, measurements of hepatocyte death help place cell loss alongside tissue repair. A death measurement can show whether an experimental condition is associated with damage while the liver is attempting to restore its tissue. Consequently, these measurements help distinguish a regenerative context from one dominated by ongoing injury, supporting interpretation of liver maintenance and repair.
In pharmaceutical and chemical safety testing, hepatocyte death measurements provide evidence of potential liver injury. Investigators can use them to compare responses to different exposures and identify whether tested substances are associated with loss of liver parenchymal cells. The resulting information contributes to toxicological interpretation by showing how an exposure affects cells central to liver tissue integrity.