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BMS2002 > strand 2 > Flashcards

strand 2 Flashcards

1
Q

tissues function

A

specialization
distribution of workload/ mechanical stress

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2
Q

4 types of animal tissues

A

epithelial
muscular
nervous
connective

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3
Q

epithelial tissue cells to ECM ratio

A

^ cells
less ECM contact

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4
Q

cell junctions

A

link individual cells

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5
Q

cytoskeletal filaments

A

transmit mechanical forces

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6
Q

basal lamina

A

point of cell attachment
connective tissue

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7
Q

characteristics of epithelial cells

A

assymetric/ polarized

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8
Q

4 types of cell junctions in tissues

A

adherins junctions
desmosomes
tight
junctions
gap junctions

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9
Q

cadherin

A

superfamily of Ca2+ dependent molecules
E-cadherin/ N cadherin/ P cadherin
classical/ non-classical

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10
Q

components of adherens junctions

A

flexible hinge region separates 5 copies of extracellular domain
N-terminal cadherin domains
Ca2+

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11
Q

adherens junctions

A

homophilic cadherin binding
E-cadherin-N-cadherin
intracellular domain interacts w actin via catenins / adaptor proteins > reducing tension as myosin II pulls on actin

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12
Q

Ca2+ function in adherens junctions

A

prevents flexing
promotes homophilic binding to another cadherin

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13
Q

macro-assembly allowing adherens junctions to withstand mechanical force

A

membrane protrusions initiate cell-cell contact
actin/ cadherin recruitment expands junction
actin remodelling/ myosin recruitment further expands

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14
Q

desmosomes

A

specialized cadherins connecting w intermediate filaments for strength at junctions

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15
Q

tight junctions

A

selective permeability barrier of epithelial
sealing strands of occludin and claudin proteins
differential transporter molecules expressed in apical/ basal PM
selective transport

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16
Q

gap junctions

A

connexin/ innexin channels

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17
Q

similarities w epithelial/ muscle/ nervous tissue

A

4 junction types
^ cell-cell interaction
basal lamina interaction

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18
Q

ECM function

A

strength and support
cell communication
polarity
shape
cell migration

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19
Q

basal lamina

A

thin layer of ECM
produced by cells above and below
evolutionarily conserved
maintains epithelial
laminin/ typeIV/ XVIII/ collagen / nidogen/ perlecan/ fibronectin

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20
Q

connective tissue

A

reduced cellular content/ cell-cell contact
^ECM content

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21
Q

ECM

A

main stress-bearing component of connective tissue
indirect means of cell-cell contact

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22
Q

2 types of connecive tissue

A

indigenous
immigrant (immune cells)

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23
Q

connective tissue ECM composition

A

^MW ^charged polysaccharides
fibrous proteins
glycoproteins
(all self-associate)
» Can become calcified/ transparent

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24
Q

polysaccharides in ECM of connective tissue

A

GAGs cov. attached to proteins (repeating sulphated disaccharide
bind much water

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25
Q

fibrous proteins in ECM of connective tissue

A

stiff, triple stranded, helical for tensile strength
collagen family

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26
Q

glycoproteins in ECM of connective tissue

A

elastins/ fibronectins

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27
Q

types of proteoglycans

A

simple
complex
(can self-aggregate)

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28
Q

connective tissue

A

decreased cellular content/ ^ECM content
main stress-bearing component for indirect cell-cell contact

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29
Q

types of cartilage

A

hyaline
fibro
elastic

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30
Q

hyaline collagen

A

chondrocyte articular joints

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31
Q

fibro collagen

A

joint capsules/ ligaments

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32
Q

elastic collagen

A

ear/ larynx

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33
Q

articular cartilage

A

TII collagen and aggrecan for strength and support

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34
Q

collagen bio-synthesis

A

synthesized in ER and processed in golgi, exocytosis release
pre-synthesized with pro-peptides that are removed to enable auto-aggregation

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35
Q

Ehlers Danlos syndrome

A

defective collagen deposition
hyperextensible joints

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36
Q

aggrecan

A

large proteoglycan
- attracts water for hydrated gel
- high charge (GAG)
- hyaluronan links aggregates

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37
Q

hydrated gel of aggrecan function

A

compression resistance
swelling pressure (turgor)
strength and support

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38
Q

chondrocyte

A

-only found in adult cartilage
-5-10% ECM vol
-RER/ golgi rich
-secrete type II collagen and aggrecan
-highly specialized indigenous cell

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39
Q

chondrocyte differentiation

A

during embryonic development from MSC

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40
Q

MSC

A

mesenchymal stem cells

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41
Q

MSC that differentiate into chondrocytes signatures

A

Sox-9 expression
Col2A expression
chondrocyte proliferation and ECM synthesis

42
Q

Sox-9

A

HMG-box DNA binding txn factor

43
Q

COL2A

A

produces collagen type II (cartilage precursor)

44
Q

what does chondrocyte proliferation require?

A

TGF-beta
fibroblast growth factor
insulin-like growth factor
parathyroid hormone related protein

45
Q

ECM

A

network of fibrous proteins and hydrated proteoglycans that surround cells in tissues
- maintained by synthesis and breakdown of matrix molecules

46
Q

proteinases

A

break down/ cleave proteins
intracellular e.g. threonine/ cysteine
extracel e.g. serine/ metallo

47
Q

degradome

A

570 genes in a genome encoding proteinases

48
Q

collagenase

A

break down collagen

49
Q

metalloproteinase family 3 minimal domains

A

catalytic (binds ZN2+)
PRE/pro (removed during secretion and activated)
haemopoxin (substrate specificity)

50
Q

3 types of metalloproteinase family

A
  • matrix metalloproteinases
  • ADAM
    -ADAMTS
51
Q

matrix metalloproteinases

A

key ECM modifier
- mediate catabolism and release/ activation of growth factors/hormones/cytokines in ECM
-Zn2+ binding catalytic
-ECM secretion as inactive pro-enzymes
- activated by pro region removal by kinases
^specificity

52
Q

ADAM

A

A disintegrin-like and metalloproteinase
(Most membrane bound)

53
Q

ADAMTS

A

ADAM with thrombospondin motifs
- secreted into ECM like MMPs
involved in catabolism of ECM

54
Q

what are metalloproteinases inhibited by?

A
  • alpha 2 macroglobulin
    -tissue inhibitors of metalloproteinases (TIMPs) > slot into active sites
55
Q

whats cleaved from ECM?
Why?

A

specific catabolic fragments and neo-epitopes
> allows for ECM breakdown monitoring

56
Q

Loading stress effect on ECM homeostasis

A

produces ECM fragments and ^ECM synthesis

57
Q

ECM remodelling functions

A

-embryonic development
-wound healing (angiogenesis and immune cell migration)
-metalloproteinase activity control]
-tumour prevention

58
Q

ECM breakdown product recognition

A

homeostatic control> integrin recognition/ signalling and inflam cytokines ^ECM synthesis
PRR recognition expressed in ECM cells

59
Q

healthy ECM maintenance

A

-ECM secretion of metalloproteinase
-ECM fragment recog (integrin/PRR)> feedback
-inflammation upon matrix damagee

60
Q

excessive ECM breakdown outcome

A

tumour migration

61
Q

types of ossification

A

intramembranous
endochondrial

62
Q

intramembranous ossification

A

conversion of mesenchymal tissue into bone

63
Q

endochondral ossification

A

conversion of cartilage to bone
(foetal development)

64
Q

ossification initiation

A

MSC-differentiated osteoblasts (chondrocytes die and cavities form)

65
Q

osteoblasts

A

cells forming bone

66
Q

what controls spatial patterning of ossification

A

morphogens (secreted signalling molecules)
via inductive signalling (m pass between cells via developing ECM)

67
Q

hedgehog protein family

A

sonic (SHH)
desert (DHH)
indian (IHH)

68
Q

positive feedback loops of hedgehog protein family

A

loops of IHH and PTHrp (skeletal morphogen)
> maintains spatial chondrocyte proliferation

69
Q

where’s PTHrp secreted

70
Q

Where’s PTHrP produced?

A

chondrocytes

71
Q

smoothened and patched interaction in presence of hedgehog

A

Hh binding to Ptch reverses inhibition of Smo> moves to nucleus and activates gene expression
Cubitus interruptus (Ci) switched off

72
Q

smoothened and patched interaction in presence of hedgehog

A

Ci cleaved and bound to repressor
genes switched off responsive to hedgehog

73
Q

long bone formation

A

cartilage catabolized and osteoid ECM calcified, trapping osteoblasts

74
Q

PTHrp role in long bone formation

A

maintains chondro proliferation/ cartilage production
prevents terminal differentiation

75
Q

IHH and PTHrP feedback in long bone formation

A

less PTHrp received further from central, therefore less IHH, therefore less PTHrP produced, therefore ^ossification

76
Q

articular cartilage

A

only chondrocytes
ECM connective tissue directs bone development in embryogenesis (permits mechanical load/art bone movement)

77
Q

osteoarthritis

A

progressive loss of ECM/ “chondrogenic phenotype” in articular cartilage without obvious cause

78
Q

osteoarthritis symptoms

A

limited joint movement/ deformity/ inflammation/ severe pain and reduced QOL
ass. w new bone formation

79
Q

gene expression in OA

A

reduced sox9 expression

80
Q

ECM homeostasis

A

loading stress > ECM fragments >ECM synthesis
integrins mediate signalling (FAK recruitment for altered gene exp)

81
Q

aggrecan stain

A

saffronin-o

82
Q

destabilisation of medial miniscus

A

miniscus cut to destabilize joints

83
Q

aggrecan breakdown

A

ADAMTS-S breaks down and ^neo-epitopes identifed w diagnostic antibodies

84
Q

aggrecanase

85
Q

collagenase

86
Q

genes behind OA

A

GDF5
RUNX2
PTHLH
SMAD3

87
Q

GDF5

A

growth factor of TGF beta fam in ECM

88
Q

RUNX2

A

master txn factor driving endochondrial ossification

89
Q

PTHLH

A

PTHrP chondrocyte growth factor
IHH secretion driven

90
Q

SMAD3

A

intracellular signalling protein in TGF beta production

91
Q

OA therapies

A

surgery
NSAIDs
identify/ target key proteinases (ADAMTS-4/5/ MMP-13)
genetic screening

92
Q

TIMP3

A

inhibits MMP-13

93
Q

common patients w RA

A

young female

94
Q

rheumatoid arthritis

A

progressive ECM/ chondrogenic phenotype loss in articular cartilage from immune cell-mediated damage

95
Q

Rheumatoid factor

A

IgM autoantibodies against IgG structural antigens (reacting w citrullinated epitopes)

96
Q

arginine PTM

A

citrulline

97
Q

ACPA

A

anti-citrullinated peptide antibodies
60% RA patients possess

98
Q

RA mediation

A

B and CD4 T cell mediated autoimmunity

99
Q

RA characteristics

A

synovium inflammation > leukocytes into tissues
autoreactive T cells activate macrophages> pro-inflam cytokines > ^MMP/ RANK ligand by fibroblasts
MMP attack tissues > osteoblast bone destroying/ joint destruction

100
Q

autoantigens recognized by CD4+ T cells in RA

A

collagen (CIA collagen induced antigen)
aggrecan (proteoglycan induced arthritis PGIA)

101
Q

RA therapies

A

NSAID
TNF-alpha target for infliximab
rituximab (kills B cells)
ACPA screening

BMS2002 (5 decks)

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