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Apoptosis

Apoptosis

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.

Caspases

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.

The Extrinsic Apoptotic Pathway

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

Phagocytosis of Apoptotic Cells

Phagocytosis of Apoptotic Cells

Cells undergoing apoptosis form apoptotic bodies that must be removed immediately to prevent inflammation, autoimmune diseases, and necrosis. Phagocytosis is carried out by professional phagocytes such as macrophages or immature dendritic cells. Non-professional phagocytes such as epithelial cells and fibroblasts also take part in this process; however, they are not as effective as professional phagocytes.
Normal cells contain receptors that prevent them from being recognized by phagocytes.

Cellular Injury V: Apoptosis and Autophagy

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

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Related Experiment Video

Updated: Jul 12, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Cytochrome c is released in a single step during apoptosis.

J C Goldstein¹, C Muñoz-Pinedo, J-E Ricci

¹La Jolla Institute for Allergy and Immunology, 10355 Science Center Dr., San Diego, CA 92121, USA.

Cell Death and Differentiation

|June 4, 2005

Summary

Cytochrome c release from mitochondria during apoptosis occurs in a single, rapid step. This process is independent of mitochondrial membrane potential changes and caspase activity.

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Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

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Related Experiment Videos

Last Updated: Jul 12, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Area of Science:

Cell Biology
Molecular Biology
Biochemistry

Background:

Cytochrome c release from mitochondria is a critical event in initiating apoptosis.
Understanding the precise kinetics and regulation of this release is crucial for studying cell death pathways.

Purpose of the Study:

To quantitatively measure the kinetics of cytochrome c release during apoptosis using fluorescent reporters.
To investigate the relationship between cytochrome c release, mitochondrial membrane potential, and caspase activity.

Main Methods:

Utilized fluorescent fusion proteins: cytochrome c-4CYS and cytochrome c-green fluorescent protein (cyt. c-GFP).
Measured cytochrome c release kinetics in single cells across various cell types and apoptotic inducers.
Assessed mitochondrial membrane potential (ΔΨm) and caspase activity in conjunction with cytochrome c release.

Main Results:

Cytochrome c release kinetics were consistent between cyt. c-4CYS and cyt. c-GFP reporters.
Cytochrome c release occurred rapidly (approx. 5 min) and was independent of significant changes in ΔΨm.
No evidence of caspase-dependent amplification or preceding ΔΨm changes was observed for cytochrome c release.

Conclusions:

A general, single-step mechanism governs cytochrome c release during apoptosis.
This release mechanism is independent of mitochondrial membrane potential fluctuations.
Cytochrome c release is not amplified by caspase activity in the studied models.