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MCM Final Exam > MCM Final - Cell Death and Adaptations > Flashcards

MCM Final - Cell Death and Adaptations Flashcards

0
Q

apoptotic bodies

A

small, membrane-bound vesicles occur from membrane blebbing from cell

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1
Q

apoptosis

A

programmed cell death

no inflammation

cell shrinks, degrades, forms apoptotic bodies, induces membrane signaling (phosphatidylserine

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2
Q

membrane signaling during apoptosis?

A

phosphatidylserine from inner leaflet to outer leaflet
-signals for phagocytes

no inflammation response**

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3
Q

necrosis

A

cell death due to trauma
-cells swells and ruptures

**leads to inflammation response

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4
Q

when does apoptosis occur?

A

eliminate unwanted cells
-development loss of cells to form digits

quality control
-get rid of nonfunctional cells

homestasis of cell death and cell division important

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5
Q

caspase

A

protease during apoptosis

active site - cysteine - cleaves target aspartic acid

synthesized as zymogen (pro-caspase)
-activated by other caspases

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6
Q

initiator caspases

A

cleave and activate downstream caspase

have CARD domain that assemble in activation complex

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7
Q

executioner caspases

A

cleave and activate other caspases and target proteins

target proteins: nuclear lamins, endonuclease inhibiting enzyme, cytoskeleton, adhesion proteins

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8
Q

endonuclease inhibiting enzyme

A

cleaved by executioner caspase in apoptosis

endonuclease is activated and can cleave DNA

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9
Q

Extrinsic Pathway

A

one type of apoptosis initiation

from an external signal

death receptor binds is activated

- recruits FADD
	- recruits initiator procaspases 8 and 10
		- DISC is formed
			- initiator caspases activate executioner
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10
Q

death receptor

A

of the tumor necrosis factor (TNF) family

homotrimer activated by homotrimer ligand

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11
Q

what happens during lymphocyte mediated cell death?

A

Fas death receptor activated by Fas ligand on lymphocyte
-juxtacrine signaling

Adaptor protein FADD recruited

- recruits procaspase 8 and 10
* *these two form the Death Inducing Signal Complex (DISC)

procaspases then activate executioner caspases

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12
Q

DISC

A

death inducing signaling complex

association of FADD with initiator procaspases 8 and 10

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13
Q

which caspases are involved in lymphocyte apoptosis (extrinsic)?

A

procaspases 8 and 10

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14
Q

Intrinsic Pathway

A

pathway of apoptosis
-result of injury (intracellular)

cytochrome c from mitochondria released into cytosol

- binds APAF-1 protease
	- oligomerizes into a heptamer called apoptosome
	- recruits initiator procaspase 9

caspase 9 recruits executioner caspases > apoptosis

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15
Q

Cytochrome C

A

released from the intermembrane space of mitochondria in response to high oxidative stress

binds APAF-1
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16
Q

APAF-1

A

binds cytochrome C

apoptotic protease

oligomerizes into a heptamer called apoptosome

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17
Q

apoptosome

A

oligermized (heptamer) APAF-1 that recruits initiator procaspase 9

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18
Q

what procaspase is involved in the intrinsic pathway of apoptosis?

A

procaspase 9

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19
Q

Bcl2 family of proteins

A

regulate apoptosis
-control release of cytochrome C

include pro-apoptotic BH123 and anti-apoptotic Bcl2

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20
Q

BH123 proteins

A

pro-apoptotic

Bax and Bak

form oligomers in the membrane and form pores for leakage of cytochrome C

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21
Q

Bak

A

BH123 protein involved in apoptosis signaling
-bound to mito membrane

form oligomer (with Bax) that is a pore for cytochrome release)

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22
Q

Bax

A

involved in the BH123 protein release of cytochrome C into the cytoplasm

translocated to mitochondria from the cytosol and associates with Bak to form a cytochrome C leak pore

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23
Q

Bcl2 proteins

A

anti-apoptotic
-bind and inhibit pro-apoptotic proteins

on the surface of mitochondria
-Bcl2 and Bcl-XI

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24
Q

BH3 only proteins

A

inhibit anti-apoptotic proteins

enable aggregation of Bax and Bak (leak pore cytochome C)

activated via signal transduction
-MAPK and p53

Bid protein activated by caspase 8

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25
Q

Bid protein

A

link between the extrinsic and intrinsic pathways of apoptosis

activated by caspase 8
-inhibits anti-apoptotic Bcl2 and stimulate pro-apoptotic BH123 proteins

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26
Q

Inhibitors of Apoptosis (IAP)

A

bind and inhibit caspases (or polyubiquitylate)

inhibit apoptosis

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27
Q

Anti-IAPs

A

released from mitochondria during intrinsic pathway

bind and inhibit IAPs - promoting apoptosis

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28
Q

survival factors

A

most cells need continuous signaling to avoid apoptosis

ex./ neurons need neurotrophins

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29
Q

necrosis

A

releases intracellular components we can detect

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30
Q

ischemia

A

inhibition of blood supply

decrease both metabolites and oxygen

acute injury

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31
Q

myocardial infarction cell death?

A

necrosis of cardiac myocytes

look for cardiac troponins and creatine kinase (CK-MB) in blood

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32
Q

apoptosis

A

clean cell death

can either have too much or too little apoptosis

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33
Q

neurodegeneration

A

due to too much apoptosis

neurons undergoing programmed cell deatah
ex/glaucoma

34
Q

glaucmoma

A

loss of visual bc apoptosis of retinal ganglion cells

cause unknown

35
Q

autoimmune disease

A

too little apoptosis
autoimmune lymphoproliferative syndrome (ALPS)
-mutation in Fas ligand
-accumulation of autoreactive lymphocytes

36
Q

cancer cells

A

resistance to apoptosis

-due to mutations in apoptosis control genes

ex/ Bcl2 (b cell lymphoma) proto-oncogene
ex/ p53 tumor supressor

37
Q

loss of p53

A

no cycle checkpoint for DNA damage
-cells with damage proliferate

cells escape apoptosis

cells can resist chemo and radiation therapy

38
Q

reversible cell injury

A

can be reversed if stimulus removed

39
Q

irreversible cell injury

A

cell is committed to cell death

40
Q

free radicals

A

unpaired electron and is highly reactive

causes chain propagation > keeps reacting

41
Q

reactive oxygen species

A

oxygen derived free radical

normal mitochondria byproduct

also from peroxisomes and lysosomes

42
Q

reactive nitrogen species

A

NO is source of RNS

-signaling species in cell

43
Q

lipid peroxidation

A

occurs at membranes

synthesizes free radicals

can become reactive peroxide (oxygen species + unsaturated FAs)

44
Q

Fenton Reaction

A

Iron reacts with H2O2 to produce hydroxyl radicals

source of ROS

45
Q

UV light and radiation

A

have ionizing properties that can form ROS

46
Q

oxidative stress

A

ROS and free radicals can lead to damage in the cell

protein modification

DNA lesion

47
Q

necrosis and ROS?

A

acute irreversible damage

48
Q

apoptosis and ROS?

A

chronic slow ROS damage

49
Q

antioxidants

A

molecules that can scavange or inactivate ROS

free unpaired electron

ex/estrogens (conjugated ring structure)

50
Q

catalase

A

H2O2 > H2O and O2

peroxisomal enzyme

51
Q

superoxide dismutase (SOD)

A

cytosolic and mitochondrial

convert superoxide to H2O2

52
Q

glutathione peroxidase

A

break H2O2 down into OH- by oxidizing itself into a homodimer

oxidized from GSSG
reduced from GSH

53
Q

GSSG

A

dimer - oxidized form of glutathione peroxidase

54
Q

GSH

A

monomer reduced form

ratio of these can detect presence of oxidative stress

55
Q

ischemia

A

insufficient blood flow
-no oxygen OR metabolic substrates

halts both aerobic AND anaerobic metabolism

56
Q

hypoxia

A

reduce in available oxygen

only affects aerobic metabolism

57
Q

anoxia

A

absence of oxygen

58
Q

mechanism of hyopxia

A

less O2 to cell
loss of aerobic metabolism > decrease ATP
1 sodium pump failure
-cell swells
2 calcium pump failure
-accumulate intracellular Ca2 (leads to activation of pathways)
-can induce apoptosis
-activates ATPases, endonuclease, proteases, phospholipases

59
Q

mechanism of ischemia

A

same as hypoxia

extra effect - no substrates for glycolysis

in addition - accumulate lactic acid (changes pH)

60
Q

Hif1

A

hypoxia-inducible factor-1

produced in response to hypoxia

promotes angiogenesis (blood vessel formation)

61
Q

Von Hippel Lindau

A

bonds to and degrades Hif-1

results in inhibition of angiogenesis

62
Q

ischemia-reperfusion injury

A

return of blood flow to hypoxic tissue is even more damaging

  • generate even more ROS (more substrates ex/Iron)
  • induces inflammation
63
Q

adaptation to stimulus

A

reversible change in a cell

64
Q

hypertrophy

A

increase in cell size

in non-dividing or senescent cells

can be caused by functional demand or stimulation signals
(growth factors)

65
Q

hypertrophy heart

A

increase in protein synthesis of proteins allowing contraction of heart

66
Q

hyperplasia

A

occurs in dividing cells

increase in cell number

not cancer

ex/ endometrium of uterus - hyperplasia is normal
however, some patients have too much hyperplasia
-leads to dysfunction

67
Q

glandular epithelial of breast

A

undergoing both hypertrophy and hyperplasia

68
Q

agenesis

A

failure to form embryonic cell mass

entire missing organ

69
Q

aplasia

A

part of organ missing

failure to differentiate into organ specific tissues

70
Q

dysgenesis

A

missing tissue of an organ

71
Q

hypoplasia

A

not growing to a full size

72
Q

atrophy

A

decrease in cell size and number

normal during development

also pathological

73
Q

involution

A

decrease in number of cell compared to the normal number

non-pathological

ex/ breast and uterus, thymus

74
Q

metaplasia

A

substitution of one cell for another
-reprogramming of stem cells due to environmental stimulus

ex/ barrets esophagus - caused by regurgitation of acid from stomach

75
Q

intracellular accumulations - categories?

A

endogenous

exogenous

76
Q

steatosis

A

accumulation of triglycerides in the cell

77
Q

atherosclerosis

A

cholesterol accumulation in the cell

78
Q

xanthoma

A

cholesterol accumulation in the cell

79
Q

protein deposits

A

can be extracellular or intracellular

80
Q

calcification

A

deposition of calcium phosphate

usually associated with dying cells (necrosis)

-intracellular calcium interacts with membrane phospholipids

81
Q

cell starvation

A

will undergo autophagy

- digest its own components
- in autophagic vacuole
82
Q

residual body

A

debris in a vacuole that we cannot digest in lysosome

83
Q

lipofuscin

A

sign of free radical injury

caused by lipid peroxidation

MCM Final Exam (16 decks)

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