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- cell “murder”
- cell swells and bursts
- PM integrity lost
- No alteration of nucleus
- Cause: toxic stimulus or acute injury
- Consequence: Tissue damage, inflammatory response induction
cell “suicide”
induction of cells intrinsic suicide program in irreparable cells
1. chromatin compaction and segregation
2. condensation of cytoplasm
3. nuclear fragmentation
4. blebbing
5. cell fragmentation
6. phagocytosed, no inflammation
Apoptosis vs. Necrosis
No leakage of cell contents
No inflammation
Not perceptible to organism
Functions of Apoptosis
Delete unwanted structures
Sculpt specific tissues
Control cell numbers (nerve cells)
Elimination of abnormal, nonfunctional or dangerous cells
Too Little Cell death
Autoimmune disorders
Viral infections
Too Much Cell Death
-Neurodegenerative d/o (alzheimers; parkinsons)
-Spinal cord injuries
-Heart Attack
Functions of Apoptosis in Adulthood
-Control cell numbers
-Eliminate damaged, mutated, or infected
-Reversible development of particular organs (birdsong)
Triggers of Apoptosis
-Withdrawal of positive signals (for continued survival)
-Receipt of negative signal (signal to die)
-Interplay of both + and – signals
Factors that Drive Apoptosis
-Bcl-2 Family members which regulate pro or anti apoptotis
-Adapters that convert pro-caspases into active proteases
-Caspases: executioner proteases
-Cysteine proteases that cleave C-side of Aspartate
-Synthesized as pro-enzymes that are converted to active form
-Specific intracellular targets, cleavage of which leads to apoptosis
Activation of caspase
-Extracellular via Fas protein and Killer T cell
-Intracellular via Cytochrome C from mitrochondria
Triggers of Ctyochrome C release from Mitochondria
-Withdrawal of survival factors
-Receptor ligand interactions (TNF)
-Cell damage
-Aging, mitochondrial DNA damage
Regulation of Cytochrome C release
BCL-2 Family
“Eat me” signal on apoptotic cell
=Phosphatidyl Serine on outer leaflet of PM
(normally only on inside)
-Phagocytotic Cells have PS receptor

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