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21 fall: Biochem > Test 3: 49 and 53 > Flashcards

Test 3: 49 and 53 Flashcards

1
Q

why do cells dies?

A

Internal and external signals

Trauma

Maintain homeostasis: cells divide and die at the same rate

Faulty cell function, such as loss of cell-cycle regulation

Developmental cues

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2
Q

what is necrosis?

A

•Death of cells and living tissue, most often accidental

cytoplasm and nucleus change

cell swells and leaks out causing inflammation

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3
Q

necrosis is caused by factors ___ to the cell

A

external

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4
Q

what are some factors that can cause necrosis

A

trauma

damaged blood vessels, hypoxia/ischemia

toxins

infection

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5
Q

what are some examples of trauma that can cause necrosis

A

•Extreme temperatures (burns, frostbite), radiation, electric shock, sudden changes in atmospheric pressure, mechanical trauma

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6
Q

what causes ischemia that leads to necrosis

A

cardiopulmonary disease, carbon monoxide poisoning

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7
Q

how does cell change during necrosis

A

cytoplasm becomes vacuolated and ER and mitochondria will swell

if cell can’t recover, cell will burst and will trigger an inflammatory response

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8
Q

Necrosis: Cell death induces nuclear changes: swelling & DNA breakdown such as ___

A

–Pyknosis, karyorrhexis, karyolysis

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9
Q

cytoplasm during necrosis will become ___

A

vacuolated (swells and little holes)

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10
Q

nuclear shrinkage

A

pyknosis

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11
Q
A

pyknois - nuclear shrinkage, DNA condenses into shrunken basophilic mass

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12
Q
A

karyorrhexis

nuclear fragmentation

pyknotic nuclei membrane ruptures and nucleus undergoes fragmentation

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13
Q

nuclear fragmentation

A

karyorrhexis

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14
Q

nuclear fading

A

karyolysis- chromatin dissolution due to action of DNAases and RNAases

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15
Q
A

karyolysis

nuclear fading

chromatin dissolution due to action of DNAases and RNAases

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16
Q

which is necrotic?

A

smear of randomly cut up DNA pieces

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17
Q

why is there a ladder?

A

apoptotic DNA gets broken into specific pieces (farther down means smaller moves faster)

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18
Q

how do cells die from necrosis

A
  1. loss of cell membrane integrity
  2. cell death products are released into extracellular space
  3. initiates inflammatory response
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19
Q

•Necrosis’ is a term used by ___ to designate presence of dead tissues or cells after death.

A

pathologists

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20
Q

___ is the sum of changes that have occurred in cells after they have died.

A

necrosis

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21
Q

•At cellular level, presence of necrosis tells us that a cell has died, but not ___ death occurred.

A

how

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22
Q

Treatment for necrosis

A

treat cause of necrosis

prevent infection, anti inflammatory

remove dead tissue to promote healing

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23
Q

summary of necrosis:

cell volume will ___

cell surface will become ___

response will be ___

A

swollen

leaky

inflammatory

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24
Q

summary of necrosis:

organelles will ___

where does necrosis occur ___

what happens to chromatin___

A

swell and disintegration

localized: contiguous cells

broken clumps

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25
Q

summary of necrosis:

onset is usually ___

enzyme cascade will ___

biosynthesis will ____

DNA fragmentation will appear as a ___ on a gel

A

accidental

truncated

loss of ion homeostasis

random smear

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26
Q

SARDS

A

sudden acquired retinal degeneration syndrome

  • Older animals (median age 8.5 yrs)
  • Pugs, Brittany spaniels, maltese predisposed•60-70% female bias
  • No inflammation, allergy, autoimmunity (?)
  • Blood/urine analysis may suggest hyper-adrenocorticism (not Cushing’s Syndrome because low cortisol high estrogen)
  • Cells of the retina (rods & cones) undergo apoptosis, resulting in sudden irreversible blindness
  • SARDS diagnosis is confirmed with retinal function test (electro-retinogram)
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27
Q

programmed cell death

A

apoptosis

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28
Q

why do we need apoptosis?

A

Development and differentiation during embryogenesis such as making fingers or deleting structure : frog tail

regulation cell numbers- Cell cycle regulation

remove defective cells or self reactive lymphocytes

Regulation and function of the immune system.

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29
Q

Adults lose ___ cells daily to apoptosis

kids lose 20-30 billion cells/day

A

50-70 billion

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30
Q

when is apoptosis inhibited

A

Cancer, developmental disorders, degenerative diseases

Autoimmune diseases (rheumatoid arthritis, lupus erythematosus) have defective apoptotic pathways

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31
Q

when is there overactive apoptosis

A

-neurodegenerative disorders, AIDS, ischemic damage

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32
Q

cellular changes with apoptosis

A

mild convolution (skinkage)

chromatin compaction and margination

condensation of cytoplasm

breakup of nuclear envelope

nuclear fragmentation

blebbing

cell fragmentation

33
Q

what happens to apoptotic cells

A

they bleb into pieces and get eaten (phagocytosis)

34
Q

what is happening?

A

apoptosis

nuclear gone

chromatin condensed

35
Q

2 types of apoptotic induction

A

intrinsic inducers

extrinsic inducers

36
Q

intrinsic inducers of apoptosis

A
  • signals originate inside the cell
  • When cell is damaged beyond repair, infected, stressed or starved
  • Results from: defective DNA repair, cytotoxic drugs, irradiation, loss of survival signals, developmental cues
  • Mitochondria
37
Q

extrinsic inducers of apoptosis

A

signals originate outside the cell

Signal is transmitted via cell surface receptors “death receptors”

Toxins, cytokines, hormones, growth factors

Positive or negative induction

38
Q

In extrinsic inducers of apoptosis, signal is transmitted via cell surface receptors “___“

A

death receptors

39
Q

what is shared in both extrinsic and intrinsic pathways of apoptosis

A

capases

40
Q

___ is a family of proteins that execute apoptotic process

A

caspases

41
Q

Caspases

A

mediate cell death

14 different members

  • Cysteine residue in catalytic site
  • Cleave after Asp residue
  • Synthesized as inactive zymogens (procaspases)
  • Initiators: caspase-8, -9, -10
  • Effectors: caspase-3, -6, -7
42
Q

which caspases are initiators of apoptosis?

A

•Initiators: caspase -8, -9, -10

43
Q

which caspases are effectors?

A

Effectors: caspase-3, -6, -7

44
Q

caspases have ___ residue in catalytic site

A

cysteine

45
Q

caspases cleave after ___ residue

A

aspartate

46
Q

how does pro-caspase become activated

A

an active caspase comes in and cleave the prodomain

they two pieces left over change shape and form active caspase

47
Q

explain caspase cascade

A

one active caspase can activate many other procaspases into active caspases

48
Q

examples of death receptors

A

FasL, TNF

transmembrane receptors that transfer signal into cell

used for extrinsic pathway of apoptosis

49
Q

2 pathways for extrinsic pathway of apoptosis (general)

A

type 1: death receptors - FasL, TNF

Type 2: mitochondria- will release cytochromeC into cytoplasm

50
Q

Direct caspase activation

A

extrinsic pathway for apoptosis

Transduction from external signal to cell death through caspase cascade

Death receptors: cell surface receptor that transmit apoptotic signals, initiated by ligands. Fas, TNF-R

Ligands: Fas ligand, Tumor Necrosis Factor (TNF)-a

51
Q

Mitochondria trigger apoptosis when ___

A

Type 2 extrinsic pathway: caspase signaling is not strong enough for execution of cell- caspase 8 will trigger mitochondria

intrinsic pathway: triggered mitochondria will release cytochromeC which which will trigger caspase 9 to cleave procaspase 3 into caspase 3 which leads to apoptosis

signal is routed through mitochondria for amplification

52
Q

Transduction from external signal to cell death through caspase cascade is ___ and uses ___

A

type 1 extrinsic signal for apoptosis

Death receptors and ligands

53
Q

caspase ___will trigger mitochondria to release cytochromeC which which will trigger caspase __ to cleave procaspase 3 into caspase 3 which leads to apoptosis

A

8

9

54
Q

DISC apoptosis

A

death inducing signaling complex

55
Q

explain how DISC is formed in apoptosis type 1

A

in extracellular space

Fas Receptor will bind to FasL (ligand)

in cytoplasm

DD( death domain) will bind to DD domain on FADD

DED (death effector domain) of the FADD will then bind to the pro-caspase 8

56
Q

how does killer lymphocyte trigger extrinsic pathway for apoptosis

A

Fas Ligand binds to Fas death receptor

this triggers FADD to bind which triggers DED (death effector domain) to bind with procaspase 8 attached

this unit of FADD, DED and procaspase is called the DISC

procaspase will get cleaved into active caspase 8

57
Q

how do mitochondria trigger apoptosis

A

intrinsic pathway

mitochondria gets injured or broken and cytochrome c breaks out

Apaf-1 will bind with cytochrome c

this will bind to procaspase 9 (apoptosome)

and activate it into

caspase 9 which will trigger a caspase cascade of 3,6,7 which will trigger apoptosis

58
Q

apoptosome

A

cytochrome c, Apaf 1 and procaspase 9

intrinsic pathway of mitochrondria

59
Q

how can mitochondria be injured

A

increased cytosolic Ca2+

oxidative stress

lipid peroxidation

60
Q

what protein regulated the release of cytochrome C from the mitochondria

A

Bcl2 protein family

61
Q

what blocks cytochrome c release from mitochondria?

A

Bcl-2 subfamily

Bcl2 and Bcl XL

(all have BH1, 2,3,4 domains)

62
Q

what act to bind and inactivate apoptotic inhibitors of mitochondria

A

Pro-apoptotic

BH3

Bid

Bim

Bad

Puma

Noxa

63
Q

what will stimulate cytochrome c release from mitochondria?

A

pro-apoptotic

Bax

Bak

(all have BH1, BH2 and BH3 domains)

64
Q

how do B proteins act on mitochondria

A

BH3 will inhibit Bcl-2 which will inhibit Bax

BH3: pro apoptotic: bind and inactivate apoptotic inhibitors

Bcl-2: inhibit apoptosis: block cytochrome c release

Bax: pro apoptotic: stimulate release of cytochrome c

65
Q

how are Bcl-2 and Bax similar

A

both have BH 1, 2 and 3 domains (Bcl-2 has BH4 as well)

tethered to outer mitochondrial membrane

66
Q

how is BH3 subfamily different from Bcl-2 subfamily and Bax subfamily

A

BH3 only has BH3 domain and is not necessarily tethered or membrane associated- missing membrane anchor)

Bcl-2 have BH 1-4, Bax have BH 1-3: both are tethered to the outer mitochondrial membrane

67
Q

stages of apoptosis that results in cell death

A
  • Disruption of mitochondrial inner membrane (MIM) potential
  • Opening of the permeability pore: small solutes leak out
  • ATP synthesis is stopped
  • Redox homeostasis is lost
  • Formation of ROS: positive feedback on loss of MIM potential
  • Influx of water ruptures mitochondrial outer membrane
  • Release of pro-apoptotic proteins–Cytochrome C
  • Nuclear DNA digestion
68
Q

how do cells actually die during apoptosis

A

destruction of key cellular proteins

recognition by phagocytic proteins

69
Q

destruction of key cellular proteins during apoptosis:

A

–Cleavage of actin & many other important targets

–DNAses cleave genomic DNA

70
Q

what is the final step of apoptosis

A

gets eaten by macrophages:

Engulfment has 5 stages

  1. sensing apoptotic cell
  2. phagocytic recognition
  3. internalization of target cell
  4. Ingestion
  5. post-engulfment response of phagocyte
71
Q

compare and contrast necrosis vs apoptosis

A
72
Q

compare necrosis vs apoptosis

cell volume

cell surface

response

A
73
Q

compare necrosis vs apoptosis

organelles

incidence

chromatin changes

A
74
Q

compare necrosis vs apoptosis

onset

enzyme cascade

biosynthesis

DNA fragmentation

A
75
Q

how can necrosis be regulated

A
  • Genetically controlled cell death
  • Results in cellular leakage
  • Cytoplasmic granulation
  • Organelle/cellular swelling

Examples:

Necroptosis

Parthanatos

Oxytosis

Pyronecrosis

Pyroptosis

76
Q

necroptosis

A

regulated necrosis

(usually accidentally but in necroptosis will happen on purpose by body)

77
Q

SARDS induced by intrinsic or extrinsic pathway?

A

could be both

intrinsic- excess Calcium triggers mitochondria to release Cytochrome C

78
Q

Why would immunosuppressants be used for treating animals that have experienced necrosis? This seems counter-intuitive.

A

A2. Yes, it does! Trauma, like toxin exposures, results in a rapid series of innate immune responses. Because necrosis results in the release of cellular molecules (which are classified as DAMPs: damage-associated molecule patterns) into the surrounding area, these molecules induce an inflammatory response. DAMPs include molecules from different cellular compartments: cytosol (e.g. uric acid, heat shock proteins, ATP), mitochondria (e.g. mtDNA, formyl peptides, ATP), nucleus (e.g. HMGB1, histones, DNA), plasma membrane (e.g. syndecans, glypicans), and endoplasmatic reticulum (e.g. calreticulin) …. The list of DAMPs is still growing. Thus, the immune system is ‘exposed’ to these DAMPs, which can escalate the innate immune response, resulting in greater inflammation, generating a viscious cycle of even more innate immune responses. This can result in organ dysfunction and systemic infection…thus its about a balance of using anti-inflammatory drugs and immune-suppressants.

21 fall: Biochem (44 decks)

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