Apoptosis

Question 1

Apoptosis

Answer 1

-energy dependent
-regulated enzymatic degradation of DNA and proteins
-shrinkage and fragmentation
-plasma membrane remains intact
-targeted and rapidly cleared by phagocytes
-no leakage of cellular contents
-no inflammatory reaction (very different than necrosis)

Question 2

Apoptosis in physiologic conditions

Answer 2

-DNA damage
-Accumulation of unfolded proteins in ER
-pathologic atrophy in parenchymal organs after duct obstruction (eg. Hydronephrosis- blockage of a ureter)
-cell death in tumours
-cell death of infected or neoplastic cells induced by cytotoxic T cells

Question 3

Morphologic characteristics of apoptosis

Answer 3

-cell shrinkage
-chromatin condensation and nuclear fragmentation
-cytoplasmic blebs and apoptotic bodies

Question 4

Mechanism of apoptosis

Answer 4

1. Initiation phase (extrinsic receptor initiated pathway OR intrinsic mitochondrial pathway)
2. Execution phase
3. Removal of dead cells (sloughed of protein buds and phagocytosis by macrophages)

Question 5

Mitochondrial (intrinsic) pathway

Answer 5

-withdrawal of growth factors, hormones
-promotes changes
-caspases (enzymes activate each other in a chain)

Question 6

Death receptor-initiated pathway (extrinsic)

Answer 6

-receptor-ligand interactions OR cytotoxic T cell activation
-activates caspases, turning on apoptosis

Question 7

Cytochrome c

Answer 7

-when released out of the membranes through damage (DNA damage mediated apoptosis), they can also stimulate the activation of caspases

Question 8

Uncleaved caspases 3 or 6

Answer 8

-inhibit apoptosis

Question 9

Cleaves caspases 3 or 6

Answer 9

-active form
-when cleaved, they allow cell to begin apoptosis and there is no going back at that point

Question 10

Dysregulated apoptosis

Answer 10

-too little or too much
>can have defective or increased apoptosis
»defective: neoplasia, autoimmune disorders
»increased: death of virus-infected cells, autoimmune disorders