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Related Concept Videos

Apoptosis01:30

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 Pathway01:31

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 Pathway01:17

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...
Translocation of Proteins into the Mitochondria01:19

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Autophagic Cell Death01:18

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 Autophagy01:22

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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Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
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Mitochondrial apoptosis is amplified through gap junctions.

Pablo M Peixoto1, Shin-Young Ryu, Dawn Pietkiewicz Pruzansky

  • 1Dept Basic Sciences, New York University College of Dentistry, New York, NY 10010, USA.

Biochemical and Biophysical Research Communications
|September 22, 2009
PubMed
Summary

Cell death can spread to nearby cells via the bystander effect. This study shows mitochondrial apoptosis triggers this effect through gap junctions, amplifying cell death signals.

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Monitoring Dynamic Changes In Mitochondrial Calcium Levels During Apoptosis Using A Genetically Encoded Calcium Sensor

Published on: April 1, 2011

Area of Science:

  • Cell Biology
  • Apoptosis Research
  • Molecular Mechanisms of Cell Death

Background:

  • The bystander effect describes how the death of one cell can induce death in neighboring cells.
  • Mitochondrial outer membrane permeabilization (MOMP) is a key event in apoptosis.
  • The role of mitochondrial apoptosis in mediating the bystander effect is not fully understood.

Purpose of the Study:

  • To investigate if mitochondrial apoptosis can induce a bystander effect.
  • To elucidate the pathway through which mitochondrial apoptosis mediates the bystander effect.
  • To explore the role of gap junctions in transmitting apoptosis signals.

Main Methods:

  • Microinjection of cytochrome c into osteoblasts to mimic mitochondrial apoptosis.
  • Exogenous expression of tBid to induce MOMP and cytochrome c release.
  • Inhibition of gap junction intercellular communication (GJIC).
  • Experiments using connexin-43 deficient osteoblasts.

Main Results:

  • Microinjection of cytochrome c induced apoptosis in both target and neighboring osteoblasts.
  • Inhibition of GJIC significantly suppressed the bystander effect.
  • Exogenous expression of tBid also triggered a bystander effect.
  • Cytochrome c microinjection in connexin-43 deficient cells only caused target cell apoptosis, confirming the role of gap junctions.

Conclusions:

  • Mitochondrial apoptosis, initiated by factors like cytochrome c release, generates a death signal.
  • This death signal is transmitted to neighboring cells via gap junctions, amplifying apoptosis.
  • The findings highlight the crucial role of gap junctions in the bystander effect mediated by mitochondrial apoptosis.
  • This mechanism has potential implications for developing novel therapeutic strategies targeting cell death.