Cell death Flashcards
(25 cards)
regulated cell death is
apoptosis
unregulated cell death is
necrosis
stages of apoptosis
commitment phase- intrinsic/extrinsic death signals commit cell to die
execution phase- morphological and biochemical changes
clearance of apoptotic cells: phagocytosis of apoptotic bodies
how is apoptosis activated?
- binding it’s ligand to death receptor
- loss of survival factors
- cell injury
death receptors are:
- cell- surface receptors
- structurally related molecules of tumour necrosis factor TNF superfamily
- death ligands bind to death receptor
activation of FAS receptor by FAS ligand (FASL) triggers:
- apoptosis in bacteria/ virus-infected, cancer and foreign cells
- deletion of activated mature T cells at the end of the immune response
cell injury are things such as:
which can then lead to:
lack of nutrients, oxygen
allergy
virus
heat cold
drugs
apoptosis and necrosis
cell injury due to dna damage
- ionising radiation or UV radiation
- p53 activation, p53 is a tumour suppression gene (ensures damaged dna is not passed on)
- controlled expression of 200-300 genes
- cell cycle arrest(dna repair) or apoptosis is damage is irreparable
cell injury whatever the cause is:
reversible or irreversible
and dependent on degree of cell damage and injury stimulus
which leads to apoptosis or necrosis
cell changes in apoptosis
- protrusions of plasma membrane
- constriction of cytoplasm
- shrinkage in cell volume
- increased cell density
nuclear changes in apoptosis
- condensation of chromatin
- disintegration of nucleoli
- condensation of nucleus
- fragmentation of nucleus
final stage of apoptosis
separation of blebs and formation of apoptotic bodies
phagocytosis
what is necrosis
total dysfunction of cell organelles
leakage of enzymes to outside environment
always cause an inflammatory reaction
safe exposure time of indirect ophthalmoscope
23-80 seconds
safe exposure time of slit lamp bio microscopy
8-21 seconds
safe exposure time of operating microscope for intraocular surgery
3 seconds
safe exposure time of overhead surgical lamps
115 - 210 seconds
what are caspases
and activation by
. intracellular proteases- fiction inside cells breaking proteins
. expressed as inactive pro enzymes- they are initially synthesised as pro caspases and need to be activated
activation:
. activated by cleavage cys after asp residues
. autoproteolysis- pro caspases activates itself
. by other active caspases
activation of caspase cascade
- death receptor and ligand interaction
- removal of survival signals
- cell injury
autocatalytic cleavage of procaspase 8
activation of caspase 8
activation of caspase 8 by mitochondria
- something bad happens in the cell such as damage
- mitochondria release cytochrome c
- combines with Apaf-1 to form apoptosome
- which activates caspase-9
- which then activates more caspases
initiators of proteolytic cascade
and what they do
1 2 8 9 10
activate effective caspases
commits cell to apoptosis
effector caspases are
3 6 7
cleave each other
cleave proteins
activate enzymes that induce dna fragmentation
dissemble cells
chromatin condensation
nuclear breakdown
which leads to cell death
regulation of apoptosis
bcl2 family proteins
inhibition(pro-survival) : block cytochrome c release in mitochondria
bcl2-subfamily
pro apoptotic: create pores in mitochondria allowing cytochrome c release
bax subfamily
BH3 subfamily
IAPS inhibitors of apoptosis proteins
bind and block caspases
p35 from baculovirus
crma from cowpox virus
