Calcium-mediated Apoptosis
Calcium-mediated Apoptosis - Related Videos
06:26
Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor
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Cited by 10 •
2011
This protocol describes a method for real-time measurement of mitochondrial calcium fluxes by fluorescent imaging. The method takes advantage of a circularly permutated YFP-based dual-excitation ratiometric calcium sensor (ratiometric pericam-mt) selectively expressed in mitochondria.
07:42
Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Cited by 15 •
2011
In this protocol, we describe the direct cytoplasmic microinjection of cytochrome c protein into fibroblasts and primary sympathetic neurons. This technique allows for the introduction of cytochrome c protein into the cytoplasm of cells and mimics the release of cytochrome c from mitochondria, which occurs during apoptosis.
01:30
Apoptosis
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2023
Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
08:20
Analysis of Apoptosis in Zebrafish Embryos by Whole-mount Immunofluorescence to Detect Activated Caspase 3
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Cited by 84 •
2013
Certain genetic perturbations or exposure to toxins can disrupt normal developmental processes leading to death of specific cell types. The analysis of activated Caspase 3 by whole-mount immunofluorescence in zebrafish embryos reveals stage- and tissue-specific localization of cells specifically undergoing apoptosis.
06:58
Synthesis of an In vivo MRI-detectable Apoptosis Probe
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Cited by 3 •
2012
Early detection of apoptosis may identify at-risk cell populations in a variety of diseases. Here we demonstrate a method to link an early apoptosis-detection protein (Annexin V) to a MRI-detectable iron oxide nanoparticle (SPIO). This method may be extended to other proteins of interest to generate MRI-detectable molecular imaging probes.
FAQs
Calcium can rise through sustained influx across the cell membrane or through release from intracellular stores. Although these sources differ, either route can contribute to excessive intracellular calcium when regulation fails. The resulting overload places stress on mitochondria and helps connect abnormal neuronal signaling with downstream events that promote cell elimination.
Mitochondrial membrane permeabilization marks a major transition from calcium stress to the molecular execution of apoptosis. Once this disruption occurs, cytochrome c can be released from mitochondria, supporting activation of caspases. These enzymes then dismantle the cell, making mitochondrial damage an important link between calcium overload and neuronal loss.
The key distinction is whether calcium signaling remains regulated or becomes sustained and excessive. Normal signaling can support cellular communication, whereas persistent elevation is associated with mitochondrial overload, membrane permeabilization, cytochrome c release, and caspase activation. Researchers therefore consider calcium duration and its relationship to these downstream events when evaluating neuronal injury.
Excitotoxic stress is connected to Calcium-mediated Apoptosis through disrupted calcium homeostasis. Excessive or prolonged calcium signaling can overload neuronal mitochondria and promote the sequence leading to cytochrome c release and caspase activity. This relationship helps explain how abnormal neuronal stimulation can progress from cellular stress toward programmed neuronal loss.
A useful investigation follows the pathway at several linked points: abnormal intracellular calcium signaling, mitochondrial overload, mitochondrial membrane permeabilization, cytochrome c release, and caspase activation. Examining these events together helps researchers determine whether calcium disruption is associated with the apoptotic sequence rather than treating calcium elevation as an isolated observation.
These neurological conditions are relevant because neuronal calcium homeostasis can become disrupted during damaging stress. Studying the pathway allows researchers to connect calcium dysregulation with mitochondrial injury and cell dismantling, while also comparing how excitotoxic stress and oxidative damage contribute to neuronal loss. The pathway can therefore guide investigation of potential therapeutic targets across these disorders.