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Biochem 2 > Seminar 3 ECM > Flashcards

Seminar 3 ECM Flashcards

1
Q

Definition of the extracellular matrix

A

A three dimensional network, which consists of proteins and carbohydrates and surrounds the cells of the connective tissues.

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2
Q

Components of ECM

A
  • Basal membrane
  • Interstitial matrix
    +) Collagen
    +) Proteoglycanes
    +) Adhesive glycoproteins
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3
Q

Structure of collagens

A
  • Repeating Gly-X-Y amino acid triplets (X is often: Pro; Y is often: Hydroxyprolin, Hydroxylysine)
  • Cofactor of Prolil-hydroxylase, Lysil-hydroxylse: Vitamine C
  • levorotatory alpha helix create one dextrorotatory triple helix
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4
Q

Function of collagen

A

providing the structure of the ECM

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5
Q

Identify 1 and 2

A

1 - Tropocollagen
2 - Procollagen

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6
Q

Identify 1 and 2

A

1 - Tropocollagen
2 - Procollagen

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7
Q

Describe Collagen macrostructure (monomers and interactions)

A
  1. Periodic organisation of collagen monomers
  2. Between monomers: cross-links, electrostatic and hydrophobic interactions
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8
Q

Name of this phenomenon

A

Cross-links in collagen

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9
Q

Cross-links can be formed between __
(3 pairs of AAs)

A
  1. Allysine – Lysine
  2. Allysine– Hydroxylysine
  3. Allysine – Histidine
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10
Q

Synthesis of collagen (8 steps)

A
  1. Synthesis of precollagen - RER
  2. Posttranslational modifications (Pro and Lys hydroxylation, Hydroxylysine glycosilation) - RER
  3. Synthesis of procollagen - RER
    4-5. Translocation into Golgi, vesicule forming
  4. Exocytosis into ECM
  5. Cleavage of procollagen (N-, C-peptidases)
  6. Creation of cross-links
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11
Q

Insufficient collagen synthesis
-> Name 2 diseases

A
  1. Scurvy
  2. Osteogenesis imperfecta
  3. Ehlers-Danlos syndrome
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12
Q

Causes of Scurvy

A
  1. Insufficient collagen synthesis
  2. Vitamine C deficit
  3. Defect in H bond and cross-link formation
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13
Q

Causes of Scurvy

A
  1. Insufficient collagen synthesis
  2. Vitamine C deficit
  3. Defect in H bond and cross-link formation
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14
Q

Symtomps of Scurvy

A

bleeding, muscle weakness, joint pain, gingivitis, acne, infectionsformation

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15
Q

Causes of Osteogenesis imperfecta

A
  1. Mutation of Type I. collagen
  2. Defect in triple helix formation
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16
Q

Symptoms of Osteogenesis imperfecta

A

bone and teeth developmental disorders, fragile bones, blue sclera

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17
Q

Insufficient collagen synthesis
-> Cause(s) of Ehlers-Danlos syndrome?

A

Lysil-hydroxylase mutation

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18
Q

Insufficient collagen synthesis
-> Symptoms of Ehlers-Danlos syndrome?

A

joint hypermobility, stretchy skin and tendons

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19
Q

Components of Proteoglycanes

A
  1. core proteins + glcosaminoglycane (GAG)
  2. Carbohydrate content: 95%
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20
Q

Structural features of proteoglycans

A

long, non branching, repetitve disaccharide units

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21
Q

Examples of glucosaminoglycane (GAG) in proteoglycans

A

chondroitin-sulfate, dermatan-sulfate, heparan-sulfate, hialuronic acid etc.

22
Q

Function of proteoglycans

A

water retention, providing the volume of ECM

23
Q

2 types of proteoglycans based on Localisation of proteoglycanes

A
  1. Matrix proteoglycanes
  2. Membrane-associated proteoglycanes
24
Q

4 examples of matrix proteoglycans

A
  1. Aggrecan (cartilage)
  2. Perlecan (basement membrane)
  3. Versican (vessels)
  4. Biglycan
25
4 examples of membrane-associated proteoglycans
1. Syndecan 2. Glypican 3. CD44 4. Thrombomodulin
26
Components and structural features of Glycoproteins
1. Carbohydrate content: 1-85% 2. Branching structure
27
Function of glycoprotein
transmembrane receptors , ECM proteins
28
An example of glycoprotein
. Fibrillin-1
29
What happen if there is a mutation in . Fibrillin-1?
Marfan syndrome
30
Components of the basement membrane
1. Type IV. collagen 2. Proteoglycanes (perlecan) 3. Adhesive glycoproteins
31
3 examples of Adhesive glycoproteins
1. Laminin-1 2. Nidogen 3. Fibronectin
32
3 types of Epidermolysis bullosa
1. Epidermolysis bullosa simplex (intraepidermal epithelial detachment) 2. Junctional epidermolysis bullosa (lamina lucida detachment) 3. Dystrophic epidermolysis bullosa (sub-lamina densa detachment)
33
2 enzymes that involve in ECM remodeling
1. Matrix metalloproteinases (MMP) 2. Tissue inhibitors of metalloproteinases (TIMP)
34
Characteristics of Matrix metalloproteinases (MMP)
1. Zn2+ dependent endopeptidases 2. Solubile or transmembrane types
35
Characteristics of Tissue inhibitors of metalloproteinases (TIMP)
1. MMP:TMP = 1:1 2. e.g. alpha-2-macroglobulin, RECK
36
Structure of matrix metalloproteinases
Common “minimal domain”: - Signal sequence - Prodomain - Catalytic domain
37
Activation of matrix metalloproteinases
38
MMPs’ role in metastasis formation
0. tumour formation, angiogenesis 1. local invasion 2. intravasation 3. transport into circulation, adhesion in small vessels 4. extravasation 5. metastasis fomation and angiogenesis (colonisation)
39
Tumour and stroma -> Cancer-associated fibroblasts (CAF) are formed in the presence of
1. Growth factors: TGF-b, PDGF 2. Inflammatory citokines: IL-6, IL-10, TNFa 3. Originated from: tumour cells, fibrocyte, endothel, pericyte, adipocyte…
40
What is the Impact of cancer-associated fibroblasts (CAF)?
1. Further growth of tumour cells 2. Angiogenesis (VEGF) 3. ECM remodeling 4. Immune suppression
41
3 cell adhesion molecules in cell-cell connections
1. Cadherins 2. Immunglobulins 3. Selectins
42
An example of cell adhesion molecules in cell-ECM connections
Integrins
43
Name 7 Activators of Tumour angiogenesis
1/ VEGF 2/ PDGF 3/ HIF-1 4/ TGF-b 5/ FGFs 6/ Angiopoetin 1 7/ MMP
44
Name 4 inhibitors of Tumour angiogenesis
1/ TIMP 2/ Thrombospondin 3/ Angiostatin 4/ Thrombostatin
45
4 steps of Wound healing and tissue regeneration
1. Haemostasis (1-2. day) 2. Inflammatory phase (1-2. day) 3. Proliferation phase (2-10. day) 4. Remodeling (1-12. month)
46
What do Throbocytes produce?
chemokins, PDGF, TGF-beta
47
Throbocytes produce: chemokins, PDGF, TGF-beta -> The role of these molecules
1. Leukocyta activation 2. Fibroblast activation
48
Myofibroblasts – mechano-regulation -> Identify
49
What does it mean if there is an Insufficient wound healing
When myofibroblasts do not die in apoptosis -> May cause Hypertrophic scar and Keloid
50
What is Fibrosis?
Pathologic tissue regeneration
51
Where can fibrosis be present?
1. Liver (cirrhosis) 2. Kidneys 3. Lungs 4. Restenosis after PTA etc.

Biochem 2 (38 decks)

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