Lesson 15: Apoptosis and Necrosis

Apoptosis vs. Necrosis

  • Necrosis:

    • Uncontrolled cell death due to injury.
    • Features: swelling, DNA condensing, disrupted plasma membranes, leakage of cell contents, inflammation in adjacent tissues.

  • Apoptosis:

    • Programmed cell death (PCD) that is genetically regulated.
    • Characteristics: cell shrinkage, fragmented nucleus, intact plasma membranes, no inflammation.
    • Serves to eliminate unneeded or damaged cells without tissue damage.

Pathways of Apoptosis

  • Intrinsic Pathway (Mitochondrial):

    • Triggered by cellular stress (DNA damage, misfolded proteins).
    • Involves mitochondrial changes (e.g., opening of Bax/Bak channels, release of cytochrome c).
    • Forms apoptosome which activates caspase-9.

  • Extrinsic Pathway (Death Receptor):

    • Initiated by extracellular signals binding to death receptors (e.g., Fas).
    • Activates caspase-8 through a signaling cascade.

  • Both pathways converge on effector caspases (caspases-3 and -7) leading to cell breakdown.

Key Features of Apoptosis

  • Caspases:
    • Initiator caspases (e.g., caspases-2, -8) activate effector caspases (caspases-3, -7).
  • Cell Breakdown:
    • Cellular components are fragmented and packaged into apoptotic bodies for phagocytosis,
    • Membrane blebbing occurs, and phosphatidylserine (PS) acts as an 'eat-me' signal for phagocytes.

Physiological Roles of Apoptosis

  • Maintains steady cell populations, particularly during:
    • Embryogenesis
    • Tissue remodeling (e.g., hormonally induced endometrial breakdown)
  • Implicated in pathologies due to excessive apoptosis (e.g., neurodegenerative diseases like Alzheimer's).