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Cell Proliferation and Survival Mechanisms Underlying Disease > Apoptosis > Flashcards

Apoptosis Flashcards

1
Q

apoptosis

A

programmed cell death

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2
Q

necrosis

A

cell death by injury

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3
Q

characteristics of apoptosis

A
  • morphological features
  • active
  • inherently programmed
  • can be initiated or inhibited by variety of stimuli
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4
Q

structural changes in apoptosis

A
  • nuclear and cytoplasmic condensation and breaking up of cell into fragments
  • apoptotic bodies are shed from epithelial lined surfaces or taken up by other cells where they are degraded by lysosomal enzymes
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5
Q

role of apoptosis in healthy adult tissues

A
  • cell turnover
  • focal elimination of cells during normal embryonic development
  • occurs spontaneously in untreated malignant neoplasma
  • participates in some types of therapeutically induced tumour regression
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6
Q

role of necrosis

A
  • triggers the inflammatory response by neutrophils, macrophages, and other cells of innate immune system
  • inflammatory system alerted by danger signals (“alarmins”) released by dying cells: DAMPs (e.g. HMG protein B1, heat shock proteins, etc.)
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7
Q

morphological features of necrosis

A
  • increasingly translucent cytoplasm
  • swelling of organelles
  • condensation of chromatin into small patches
  • increased cell volume leading to disruption of plasma membrane
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8
Q

morphological characteristics of dying cells

A
  • shrinkage
  • membrane blebbing
  • fragmentation
  • nuclear condesnation
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9
Q

why do cells undergo apoptosis

A
  • serious damage that cannot be repaired or requires too much energy to repair
  • outlived usefulness (e.g. shutdown of cytotoxic T-cells during immune response occurs via apoptosis)
  • become senescent (old)
  • necessary to reach final form in embryonic development
  • necessary for maintaining normal physiological processes in organism
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10
Q

normal physiological processes maintained by apoptosis

A
  • countebalancing cell proliferation to maintain homeostasis in rapidly reneqing tissues
  • mammary gland involution at weaning
  • shedding of uterine lining each month in females
  • matching number of neurons with targets
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11
Q

role of apoptosis in sculpting tissues

A
  • paw in mouse embryo: interdigital cell death eliminates tissue between developing digits
  • as a tadpole becomes a frog all tail cells are deleted
  • human embryos are thought to use apoptosis to remove webbing between digits
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12
Q

knockout Bak and Bax gene mice

A
  • Bak and Bax are functionally redundant apoptosis genes
  • webbing is not removed and paw does not develop normally
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13
Q

role of apoptosis in neuronal development

A

in embryo lacking “caspase-9” (key apoptosis gene), there was an overgrowth of the brain due to thickened ventricle walls with no cavitation (hollow space under ventricle wall)

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13
Q

role of apoptosis in neuronal development

A

in embryo lacking “caspase-9” (key apoptosis gene), there was an overgrowth of the brain due to thickened ventricle walls with no cavitation (hollow space under ventricle wall)

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14
Q

apoptosis in the eye

A

lens consists of apoptotic cells that repace innards with clear protein crystallin

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15
Q

apoptosis in skin

A
  • skin cells migrate to surface in layers, undergoing apoptosis on the way
  • resulting dead cell layer forms the protective outer skin layer, called the epidermis
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16
Q

apoptosis in thymus

A

T-cells that are ineffective or would attack the body’s own tissues commit suicide before they can enter bloodstream

17
Q

apoptosis in uterus

A

cells of the uterine wall die and are sloughed off dring menstruation by apoptosis

18
Q

apoptosis in other cells

A
  • infected cells (by virus or genetic mutations) often commit suicide
  • failure of genetically altered cell to commit suicide can contribute to development of cancer
19
Q

what is syndactyly

A

when the cells in the interdigital space fail to undergo apoptosis with the outcome that the foetus will be born with webbed feet and/or hands

20
Q

how does too little apoptosis contribute to disease

A
  • cancer (establishment, metastasis, treatment failure)
  • autoimmune disorders
  • viral infection
21
Q

how does too much apoptosis contribute to disease

A
  • neurodegenerative diseases (alzhimers, parkinsons)
  • viral infection (HIV)
  • ischemic injury
22
Q

caspases

A
  • cystine-dependent aspartate-drected proteases
  • cleave substrates after an aspartate residue at c-terminal side witbhin an appropriate recognition sequence
  • vast number of proteins are cleaved during apoptosis
  • cleavage of any one protein probably does not trigger cell death
23
Q

what could be a reason for “innocent bystander” cleavages in apoptosis

A

the relatively short cleavage sequence of caspases

24
Q

how can apoptosis be induced extrinsically

A

through ligand/receptor interactions (e.g. T-cells inducing targets to commit suicide)

25
Q

how are initiator caspases activated

A
  • activated by protein:protein interactions
26
Q

how are effector caspases activated

A
  • activated by proteolytic cleavage
27
Q

synthesis of caspases

A
  • inactive proenzymes that are processed to form active enzymes
28
Q

activation of the caspase cascade in apoptosis

A
  • pro-apoptotic signal -> initiator caspase via autocatalytic processing triggered by co-factor binding and/or oligomerisation
  • initiator caspase -> effector caspase via processing by initiator caspase
  • effector caspase -> death via cleavage of many substrates
29
Q

extrinsic apoptotic pathway

A
  • death receptor
  • FADD
  • caspase 8
  • caspase 3
  • apoptosis
30
Q

intrinsic apoptotic pathway

A
  • drugs
  • cytochrome c
  • apaf1
  • caspase 9
  • caspase 3
  • apoptosis
31
Q

how do initiator caspases get dimerised and activated

A
  • extrinic pathway
  • death-receptor mediated apoptotic pathway
32
Q

activation platform for caspase-8

A
  • DISC (death-inducing signalling complex)
  • death receptor and adapter protein FADD -> leads to recruitment of caspase 8 to the complex
33
Q

extrinsic pathway

A
34
Q

what regulates mitochondrial permeabilisation

A

Bcl-2 family proteins

35
Q

pro-survival Bcl-2 family members

A

-BCL-2
- BCL-XL
- BCL-W
- A1/BFL-1
- MCL-1
- BOO

36
Q

pro-apoptotic Bcl-2 family members

A
  • BAX
  • BOK
  • BCL-HS
  • BAK
  • BCL-CL
  • BFK
37
Q

pro-apoptotic Bcl-2 family members (BH3 only)

A
  • PUMA
  • BAD
  • BIK
  • HRK
  • BIM
  • NOXA
  • BMF
38
Q

how Bcl-2 family members regulate apoptosis and cell survival

A
  • pro-apoptotic act to initiate cytochrome c release
  • pro-survival act to inhibit cytochrome c release
39
Q

regions of anti-apoptotic Bcl-2 proteins

A

BH4, BH3, BH1, BH2, TM

40
Q

regions of pro-apoptotic Bcl-2 proteins

A

BH3, BH1, BH2, TM (or BH3 only)

41
Q

Bax and Bak activation in MOMP

A
  • ## mitochondrial outer membrane permeabilisation

Cell Proliferation and Survival Mechanisms Underlying Disease (11 decks)

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