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strand 2 Flashcards

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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
fibrous proteins in ECM of connective tissue
stiff, triple stranded, helical for tensile strength collagen family
26
glycoproteins in ECM of connective tissue
elastins/ fibronectins
27
types of proteoglycans
simple complex (can self-aggregate)
28
connective tissue
decreased cellular content/ ^ECM content main stress-bearing component for indirect cell-cell contact
29
types of cartilage
hyaline fibro elastic
30
hyaline collagen
chondrocyte articular joints
31
fibro collagen
joint capsules/ ligaments
32
elastic collagen
ear/ larynx
33
articular cartilage
TII collagen and aggrecan for strength and support
34
collagen bio-synthesis
synthesized in ER and processed in golgi, exocytosis release pre-synthesized with pro-peptides that are removed to enable auto-aggregation
35
Ehlers Danlos syndrome
defective collagen deposition hyperextensible joints
36
aggrecan
large proteoglycan - attracts water for hydrated gel - high charge (GAG) - hyaluronan links aggregates
37
hydrated gel of aggrecan function
compression resistance swelling pressure (turgor) strength and support
38
chondrocyte
-only found in adult cartilage -5-10% ECM vol -RER/ golgi rich -secrete type II collagen and aggrecan -highly specialized indigenous cell
39
chondrocyte differentiation
during embryonic development from MSC
40
MSC
mesenchymal stem cells
41
MSC that differentiate into chondrocytes signatures
Sox-9 expression Col2A expression chondrocyte proliferation and ECM synthesis
42
Sox-9
HMG-box DNA binding txn factor
43
COL2A
produces collagen type II (cartilage precursor)
44
what does chondrocyte proliferation require?
TGF-beta fibroblast growth factor insulin-like growth factor parathyroid hormone related protein
45
ECM
network of fibrous proteins and hydrated proteoglycans that surround cells in tissues - maintained by synthesis and breakdown of matrix molecules
46
proteinases
break down/ cleave proteins intracellular e.g. threonine/ cysteine extracel e.g. serine/ metallo
47
degradome
570 genes in a genome encoding proteinases
48
collagenase
break down collagen
49
metalloproteinase family 3 minimal domains
catalytic (binds ZN2+) PRE/pro (removed during secretion and activated) haemopoxin (substrate specificity)
50
3 types of metalloproteinase family
- matrix metalloproteinases - ADAM -ADAMTS
51
matrix metalloproteinases
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
ADAM
A disintegrin-like and metalloproteinase (Most membrane bound)
53
ADAMTS
ADAM with thrombospondin motifs - secreted into ECM like MMPs involved in catabolism of ECM
54
what are metalloproteinases inhibited by?
- alpha 2 macroglobulin -tissue inhibitors of metalloproteinases (TIMPs) > slot into active sites
55
whats cleaved from ECM? Why?
specific catabolic fragments and neo-epitopes > allows for ECM breakdown monitoring
56
Loading stress effect on ECM homeostasis
produces ECM fragments and ^ECM synthesis
57
ECM remodelling functions
-embryonic development -wound healing (angiogenesis and immune cell migration) -metalloproteinase activity control] -tumour prevention
58
ECM breakdown product recognition
homeostatic control> integrin recognition/ signalling and inflam cytokines ^ECM synthesis PRR recognition expressed in ECM cells
59
healthy ECM maintenance
-ECM secretion of metalloproteinase -ECM fragment recog (integrin/PRR)> feedback -inflammation upon matrix damagee
60
excessive ECM breakdown outcome
tumour migration
61
types of ossification
intramembranous endochondrial
62
intramembranous ossification
conversion of mesenchymal tissue into bone
63
endochondral ossification
conversion of cartilage to bone (foetal development)
64
ossification initiation
MSC-differentiated osteoblasts (chondrocytes die and cavities form)
65
osteoblasts
cells forming bone
66
what controls spatial patterning of ossification
morphogens (secreted signalling molecules) via inductive signalling (m pass between cells via developing ECM)
67
hedgehog protein family
sonic (SHH) desert (DHH) indian (IHH)
68
positive feedback loops of hedgehog protein family
loops of IHH and PTHrp (skeletal morphogen) > maintains spatial chondrocyte proliferation
69
where's PTHrp secreted
DHH
70
Where's PTHrP produced?
chondrocytes
71
smoothened and patched interaction in presence of hedgehog
Hh binding to Ptch reverses inhibition of Smo> moves to nucleus and activates gene expression Cubitus interruptus (Ci) switched off
72
smoothened and patched interaction in presence of hedgehog
Ci cleaved and bound to repressor genes switched off responsive to hedgehog
73
long bone formation
cartilage catabolized and osteoid ECM calcified, trapping osteoblasts
74
PTHrp role in long bone formation
maintains chondro proliferation/ cartilage production prevents terminal differentiation
75
IHH and PTHrP feedback in long bone formation
less PTHrp received further from central, therefore less IHH, therefore less PTHrP produced, therefore ^ossification
76
articular cartilage
only chondrocytes ECM connective tissue directs bone development in embryogenesis (permits mechanical load/art bone movement)
77
osteoarthritis
progressive loss of ECM/ "chondrogenic phenotype" in articular cartilage without obvious cause
78
osteoarthritis symptoms
limited joint movement/ deformity/ inflammation/ severe pain and reduced QOL ass. w new bone formation
79
gene expression in OA
reduced sox9 expression
80
ECM homeostasis
loading stress > ECM fragments >ECM synthesis integrins mediate signalling (FAK recruitment for altered gene exp)
81
aggrecan stain
saffronin-o
82
destabilisation of medial miniscus
miniscus cut to destabilize joints
83
aggrecan breakdown
ADAMTS-S breaks down and ^neo-epitopes identifed w diagnostic antibodies
84
aggrecanase
ADAMTSS
85
collagenase
MMP-13
86
genes behind OA
GDF5 RUNX2 PTHLH SMAD3
87
GDF5
growth factor of TGF beta fam in ECM
88
RUNX2
master txn factor driving endochondrial ossification
89
PTHLH
PTHrP chondrocyte growth factor IHH secretion driven
90
SMAD3
intracellular signalling protein in TGF beta production
91
OA therapies
surgery NSAIDs identify/ target key proteinases (ADAMTS-4/5/ MMP-13) genetic screening
92
TIMP3
inhibits MMP-13
93
common patients w RA
young female
94
rheumatoid arthritis
progressive ECM/ chondrogenic phenotype loss in articular cartilage from immune cell-mediated damage
95
Rheumatoid factor
IgM autoantibodies against IgG structural antigens (reacting w citrullinated epitopes)
96
arginine PTM
citrulline
97
ACPA
anti-citrullinated peptide antibodies 60% RA patients possess
98
RA mediation
B and CD4 T cell mediated autoimmunity
99
RA characteristics
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
autoantigens recognized by CD4+ T cells in RA
collagen (CIA collagen induced antigen) aggrecan (proteoglycan induced arthritis PGIA)
101
RA therapies
NSAID TNF-alpha target for infliximab rituximab (kills B cells) ACPA screening

BMS2002 (5 decks)

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