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Questions and Answers
In follicular lymphoma, the overexpression of BCL-2 prevents apoptosis, leading to increased cell survival. Which of the following mechanisms best describes how BCL-2 achieves this?
In follicular lymphoma, the overexpression of BCL-2 prevents apoptosis, leading to increased cell survival. Which of the following mechanisms best describes how BCL-2 achieves this?
- By directly interacting with death receptors, such as Fas and TNF receptors, to initiate the extrinsic apoptotic pathway.
- By promoting the formation of apoptotic bodies, facilitating the engulfment of cellular debris by macrophages.
- By inhibiting the release of cytochrome C from the mitochondria, thus preventing apoptosome formation. (correct)
- By directly activating caspases, initiating the caspase cascade and promoting cell breakdown.
A researcher is investigating potential therapeutic targets for neurodegenerative diseases characterized by abnormal protein accumulation. Based on the information provided, which of the following strategies would be most effective in promoting the removal of damaged cells?
A researcher is investigating potential therapeutic targets for neurodegenerative diseases characterized by abnormal protein accumulation. Based on the information provided, which of the following strategies would be most effective in promoting the removal of damaged cells?
- Overexpression of BCL-2 to enhance cell survival and prevent apoptosis.
- Knockdown of BCL-2 to promote cytochrome C release and caspase activation. (correct)
- Upregulation of TNF-alpha to directly induce necrosis.
- Inhibition of caspase-3 to prevent the execution of apoptosis.
During a study of liver pathology, a pathologist observes a liver biopsy from a patient with viral hepatitis. Which specific set of morphological features would the pathologist expect to see in hepatocytes undergoing apoptosis?
During a study of liver pathology, a pathologist observes a liver biopsy from a patient with viral hepatitis. Which specific set of morphological features would the pathologist expect to see in hepatocytes undergoing apoptosis?
- Karyolysis, cytoplasmic fragmentation, and loss of membrane integrity.
- Cellular swelling, karyolysis, and neutrophil infiltration.
- Pyknosis, eosinophilic cytoplasm, and karyorrhexis. (correct)
- Cellular shrinkage, basophilic cytoplasm, and extensive inflammation.
In the context of cellular response to irreversible injury, what key feature distinguishes apoptosis from necrosis, particularly concerning the inflammatory response?
In the context of cellular response to irreversible injury, what key feature distinguishes apoptosis from necrosis, particularly concerning the inflammatory response?
A researcher is comparing the intrinsic and extrinsic pathways of apoptosis. Which statement correctly differentiates the key initiating events of these two pathways?
A researcher is comparing the intrinsic and extrinsic pathways of apoptosis. Which statement correctly differentiates the key initiating events of these two pathways?
Following a viral infection, cytotoxic T cells induce apoptosis in infected cells via the extrinsic pathway. Which molecular interaction directly initiates this process?
Following a viral infection, cytotoxic T cells induce apoptosis in infected cells via the extrinsic pathway. Which molecular interaction directly initiates this process?
During apoptosis, specific enzymes dismantle the cell in a highly regulated manner. What is the critical role of caspase-3 in this process?
During apoptosis, specific enzymes dismantle the cell in a highly regulated manner. What is the critical role of caspase-3 in this process?
In a scenario where BCL-2 is knocked down in a cell, what is the immediate downstream effect on the intrinsic pathway of apoptosis?
In a scenario where BCL-2 is knocked down in a cell, what is the immediate downstream effect on the intrinsic pathway of apoptosis?
A researcher is studying the morphological changes associated with apoptosis and necrosis. Which of the following features is exclusively observed in necrosis but not in apoptosis?
A researcher is studying the morphological changes associated with apoptosis and necrosis. Which of the following features is exclusively observed in necrosis but not in apoptosis?
Macrophages recognize and phagocytose apoptotic bodies through specific signals. Which signal is primarily responsible for targeting apoptotic cells for engulfment by macrophages?
Macrophages recognize and phagocytose apoptotic bodies through specific signals. Which signal is primarily responsible for targeting apoptotic cells for engulfment by macrophages?
Flashcards
Apoptosis
Apoptosis
Cell death where activated enzymes cause a clean cell death, without an inflammatory response.
Cell Aging
Cell Aging
Cell death due to irreversible cell injury/pathological states, which can result in necrosis/apoptosis.
Intrinsic Pathway
Intrinsic Pathway
The mitochondrial pathway of apoptosis.
Extrinsic Pathway
Extrinsic Pathway
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BAX and BAK
BAX and BAK
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BCL-2
BCL-2
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Pyknosis
Pyknosis
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Karyorrhexis
Karyorrhexis
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Karyolysis
Karyolysis
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Apoptotic Bodies
Apoptotic Bodies
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Study Notes
- Apoptosis is a form of cell death where cells "fall off" in a normal fashion
- Irreversible cell injury can lead to either necrosis or apoptosis
Apoptotic Mechanisms
- Activated cell enzymes, specifically the caspase cascade, cause a clean cell death
- Apoptosis is not associated with an inflammatory response
- Two main routes exist: an intrinsic (mitochondrial) pathway and an extrinsic (death receptor) pathway
Intrinsic Pathway
- The intrinsic pathway is purely mitochondrial
- BAX and BAK, part of the BCL-2 family, facilitate cytochrome c exiting the mitochondria and binding to Apaf-1
- This binding results in apoptosome production
- Apoptosomes cleave pro-caspase-9, initiating the caspase cascade
BCL-2
- BCL-2 is an anti-apoptotic mitochondrial protein that promotes cell survival
- Follicular lymphoma overexpresses BCL-2, preventing apoptosis and promoting cell survival
Caspase Cascade
- Caspase-9 is activated, which then triggers caspase-3
- Activation of the caspase cascade leads to the breakdown of cells, cellular organelles, and the cytoskeleton, forming apoptotic bodies
Extrinsic Pathway
- The extrinsic pathway involves death receptors like Fas and TNF receptors
- T cells interact with infected cells, initiating apoptosis
Morphologic Changes
- Nuclear changes include pyknosis (nuclear chromatin condensation and shrinkage) and karyorrhexis (nuclear fragmentation)
- In karyorrhexis, endonucleases fragment the nucleus
- Pyknosis and karyorrhexis are present in both apoptosis and necrosis
- Karyolysis is only present in necrosis, involving the fading away of the nucleus
- Membrane blebbing and cytoplasmic fragmentation occur, forming apoptotic bodies
- Phospholipids are released, signaling macrophages to phagocytose the apoptotic bodies
Causes of Apoptosis
- Physiologic causes include normal aging cells undergoing apoptosis
- Pathologic causes include viral hepatitis, where cells exhibit pyknosis and eosinophilic cytoplasm (apoptotic cells)
- Huntington's disease, where accumulation of Huntington protein damages neurons
Apoptosis vs. Necrosis
- Karyolysis is unique to necrosis
- BCL-2 is an anti-apoptotic mechanism; knocking down BCL-2 promotes apoptosis
- Chromatin condensation occurs before fragmentation in apoptosis
Membrane Integrity
- In apoptosis, membrane integrity is largely maintained; membrane blebbing occurs, forming apoptotic bodies that are phagocytosed by macrophages without releasing the cell's contents
- Necrosis involves loss of membrane integrity, leading to cytoplasmic spilling, inflammation, and damage to neighboring cells
- Apoptosis is a "clean" form of cell death compared to the chaotic and harmful necrosis
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