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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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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...
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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...
Apoptosis01:30

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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.
Overview of Cell Death01:30

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Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
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Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
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Endogenous zinc mediates apoptotic programmed cell death in the developing brain.

Eunsil Cho1, Jung-Jin Hwang, Seung-Hee Han

  • 1Asan Institute for Life Sciences, Asan Medical Center, Seoul, Republic of Korea.

Neurotoxicity Research
|July 18, 2009
PubMed
Summary

Endogenous zinc accumulation precedes programmed cell death (PCD) in developing rat brains. Chelating intracellular zinc with TPEN significantly reduced neuronal apoptosis, suggesting zinc mediates this crucial developmental process.

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Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Endogenous zinc plays a role in programmed cell death (PCD) in the developing brain.
  • Intracellular accumulation of labile zinc is observed in neurons undergoing PCD.

Purpose of the Study:

  • To investigate the role of intracellular labile zinc in developmental apoptosis.
  • To determine if chelating intraneuronal zinc can prevent neuronal PCD.

Main Methods:

  • Subcutaneous injection of the zinc chelator TPEN into postnatal rats for 7 days.
  • Assessment of neuronal apoptosis frequency.
  • Analysis of caspase-9, caspase-3, Bax, and Bcl-2 expression.

Main Results:

  • TPEN treatment significantly decreased the frequency of apoptotic neurons.
  • Intracerebral zinc chelation did not alter the expression of zinc-regulating proteins (ZnT-1, ZnT-3) or synaptophysin.
  • TPEN treatment reduced activating cleavages of caspase-9 and -3 and Bax expression, while increasing Bcl-2 expression.

Conclusions:

  • Intracellular zinc acts as a key mediator of developmental apoptosis in the brain.
  • Zinc chelation may arrest PCD by interfering with the caspase-dependent apoptotic pathway.
  • This study provides in vivo evidence that endogenous labile zinc causes neuronal apoptosis.