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
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