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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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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. 
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Proinflammatory apoptosis.

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Apoptotic cells remaining in the epithelium trigger inflammation. These cells release adenosine triphosphate (ATP), a danger signal that activates inflammatory responses.

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Area of Science:

  • Cell biology
  • Immunology
  • Epithelial biology

Background:

  • Apoptosis is programmed cell death, crucial for tissue homeostasis.
  • Failure in apoptotic cell clearance can lead to inflammatory conditions.
  • Epithelial cells form barriers and are constantly renewing.

Purpose of the Study:

  • To investigate the role of uncleared apoptotic cells in epithelial inflammation.
  • To identify the molecular mechanisms by which apoptotic cells induce inflammation.

Main Methods:

  • Utilized in vitro epithelial models.
  • Employing techniques to induce and prevent apoptotic cell clearance.
  • Measured inflammatory mediator release and signaling pathways.

Main Results:

  • Apoptotic cells retained within the epithelium release significant amounts of adenosine triphosphate (ATP).
  • Extracellular ATP from these cells activates purinergic receptors on neighboring epithelial and immune cells.
  • This activation initiates pro-inflammatory signaling cascades.

Conclusions:

  • Uncleared apoptotic cells in the epithelium are a source of inflammatory signals.
  • ATP release by these cells is a key mechanism driving inflammation.
  • Targeting ATP signaling could offer therapeutic strategies for epithelial inflammation.