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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.

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Related Experiment Video

Updated: Jul 24, 2026

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization

Published on: January 13, 2012

Cell-specific caspase expression by different neuronal phenotypes in transient retinal ischemia.

M Singh¹, S I Savitz, R Hoque

¹Department of Neurology, Albert Einstein College of Medicine, Bronx, New York, USA.

Journal of Neurochemistry

|April 12, 2001

Summary

Inhibition of caspases 2 and 3 protects retinal neurons from death after ischemia-reperfusion injury. This caspase inhibition preserves retinal structure and improves function, offering a potential therapeutic strategy for vision loss.

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Last Updated: Jul 24, 2026

Monitoring Cleaved Caspase-3 Activity and Apoptosis of Immortalized Oligodendroglial Cells using Live-cell Imaging and Cleaveable Fluorogenic-dye Substrates Following Potassium-induced Membrane Depolarization

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Published on: January 13, 2012

A Mouse Model of Retinal Ischemia-Reperfusion Injury Through Elevation of Intraocular Pressure

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Published on: July 14, 2016

Quantification of Immunostained Caspase-9 in Retinal Tissue

Quantification of Immunostained Caspase-9 in Retinal Tissue

Published on: July 25, 2022

Area of Science:

Neuroscience
Ophthalmology
Cell Biology

Background:

Caspases play a role in neuronal death after ischemia-reperfusion injury.
The specific roles of caspases in retinal neuronal degeneration are not fully understood.

Purpose of the Study:

To investigate the involvement of caspases 1, 2, and 3 in neuronal death following transient retinal ischemia.
To determine if caspase inhibition offers neuroprotection in a model of retinal ischemia-reperfusion injury.

Main Methods:

Transient global retinal ischemia was induced in an animal model.
Spatial and temporal expression of active caspases 1, 2, and 3 were analyzed using cell-specific markers.
Animals were treated with various caspase inhibitors before ischemia induction.

Main Results:

Sixty minutes of ischemia caused delayed neuronal death in inner retinal layers by 7 days.
Caspase 1 was not detected; caspase 2 and 3 expression peaked at 24 hours in specific retinal neurons.
Inhibition of caspase 2 or pan-caspase activity significantly improved retinal histology and function (electroretinogram).

Conclusions:

Ischemia-reperfusion injury activates distinct caspases based on retinal neuronal phenotype.
Caspase inhibition (specifically targeting caspase 2 or broad caspase activity) provides significant neuroprotection and functional recovery.
Caspases 2 and 3 may act in parallel in amacrine neurons, suggesting potential therapeutic targets for ischemic retinopathies.