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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.

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...

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...

Autophagic Cell Death

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...

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...

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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Synchronized turbo apoptosis induced by cold-shock.

J H Fransen¹, J W Dieker, L B Hilbrands

¹Nephrology Research Laboratory, Nijmegen Center for Molecular Life Sciences, Department of Nephrology, Radboud University Nijmegen Medical Center, Nijmegen, The Netherlands.

Apoptosis : an International Journal on Programmed Cell Death

|October 26, 2010

Summary

We developed a rapid cold-shock method to generate synchronized apoptotic cells for studying systemic lupus erythematosus (SLE). This technique efficiently produces homogeneous early and late apoptotic cells and blebs for research.

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Area of Science:

Cell Biology
Immunology
Pathogenesis of Autoimmune Diseases

Background:

Apoptosis plays a role in systemic lupus erythematosus (SLE) pathogenesis.
Understanding the effects of apoptotic cells on antigen-presenting cells is crucial for SLE research.
Generating synchronized, homogeneous populations of early and late apoptotic cells in vitro is challenging.

Purpose of the Study:

To develop a rapid, reproducible method for generating synchronized homogeneous populations of early and late apoptotic cells and blebs.
To investigate the characteristics of cold-shock-induced apoptosis.
To assess the utility of these apoptotic cells in SLE-related research.

Main Methods:

Granulocytic 32Dcl3 cells were incubated on ice for 2 hours, then rewarmed at 37°C.
Apoptosis was induced via cold-shock followed by rewarming.
Apoptotic cells and blebs were characterized using Annexin V and propidium iodide staining.
Caspase activity and chromatin cleavage were assessed.
Binding of SLE-derived anti-chromatin autoantibodies to blebs was evaluated.

Main Results:

Cold-shock followed by rewarming rapidly induced synchronized apoptosis in 32Dcl3 cells.
80-90% early apoptotic cells (Annexin V+/PI-) were observed after 30-90 minutes at 37°C.
98% late apoptotic/necrotic cells (Annexin V+/PI+) were observed after 24 hours.
Apoptotic blebs formed within 20 minutes at 37°C.
Inter-nucleosomal chromatin cleavage and caspase activation were confirmed.
Caspase inhibition blocked apoptosis.
SLE-derived anti-chromatin autoantibodies showed high affinity for cold-shock-induced blebs.

Conclusions:

Cold-shock is an effective, non-toxic method for rapidly generating synchronized, homogeneous apoptotic cell populations.
This method provides a valuable tool for studying apoptosis in various contexts, including SLE pathogenesis.
The generated apoptotic blebs are recognized by SLE-specific autoantibodies, suggesting relevance for disease mechanisms.