Apoptosis
Types of Cell Death
- Cell death by injury
- Mechanical damage
- Exposure to toxic chemicals
- Cell death by suicide
- External signals
- Internal signals
Necrosis vs Apoptosis
- Necrosis
- Cellular swelling
- Membranes are broken
- ATP is depleted
- Cell lyses, eliciting an inflammatory reaction
- DNA fragmentation is random, or smeared
- In vivo, whole areas of the tissue are affected
- Apoptosis
- Cellular condensation
- Membranes remain intact
- Requires ATP
- Cell is phagocytosed, no tissue reaction
- Ladder-like DNA fragmentation
- In vivo, individual cells appear affected
Why Should A Cell Commit Apoptosis?
- Apoptosis is needed for proper development
- Embryonic Morphogenesis
- The resorption of the tadpole tail
- The formation of the fingers and toes of the fetus
- The sloughing off of the inner lining of the uterus
- The formation of the proper connections between neurons in the brain
- Regulation of cell viability by hormones and growth factors (most cells die if they fail to receive survival signals from other cells)
- Apoptosis is needed to destroy cells
- Cells infected with viruses
- Cells of the immune system
- Cells with DNA damage
- Cancer cells
What Makes a Cell Decide to Commit To Apoptosis?
- Withdrawal of positive signals
- Examples :
- Growth factors for neurons
- Interleukin-2 (IL-2)
- Receipt of negative signals
- Examples :
- Increased levels of oxidants within the cell
- Damage to DNA by oxidants
- Death activators :
- Tumor necrosis factor alpha (TNF-α)
- Lymphotoxin (TNF-β)
- Fas ligand (FasL)
Caspases
- Caspases: specialized proteases that mediate apoptosis
- Protease with cysteine at active sites
- Cleave substrates at specific aspartic acids
- Synthesized as procaspases and activated by other caspases
Caspase Activation Amplification Cascade
- An inhibitor of a DNAse: leads to fragmentation of DNA
- Nuclear Lamina: leads to fragmentation of nucleus
- Other Cytoskeletal Associated Proteins: leads to disruption of cytoskeleton and cell fragmentation
- Additional Caspases
Main Pathways Regulating Caspase Activation During Apoptosis
- Intrinsic Pathway- Mitochondrial Mediated Major Pathway in Mammalian Cells
- Outer Mitochondrial Membrane Permeabilization (MOMP)
- Release of Cytochrome C from Mitochondrial Intermembrane Space into Cytosol
- Apoptosome formation: Activation of Initiator Caspase
- Effector caspases activated
- Extrinsic Pathway- Signaling through Death Receptors
- Ligand Bound Death Receptors
- Adaptor Protein Association
- Initiator Caspase Recruitment and Activation
- Used by Immune System
Critical Regulators of Cell Death
- Bcl-2 Family– Regulate whether MOMP Occurs
- Anti-Apoptotic Factors: death inhibitors
- Function to inhibit MOMPs (Mitochondrial Outer Membrane Permeabilization) by pro apoptotic factors (aka death activators)
- Pro-Apoptotic Factors: death activators
- Bind and inhibit death inhibitors
- Directly cause MOMP to stimulate release of cytochrome C (BAX AND BAK)
- IAP Family (Inhibitor of Apoptosis)
- Bind Procaspases prevent activation
- Bind Caspases and inhibit Activity
Survival Factors
- When cells are deprived of survival factors, they activate programmed cell death pathway
- Survival factors usually act by binding to cell surface receptors
- Turn on signaling pathways that suppress cell death program
- Some increase production of Bcl2