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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
Q

4 examples of membrane-associated proteoglycans

A
  1. Syndecan
  2. Glypican
  3. CD44
  4. Thrombomodulin
26
Q

Components and structural features of Glycoproteins

A
  1. Carbohydrate content: 1-85%
  2. Branching structure
27
Q

Function of glycoprotein

A

transmembrane receptors , ECM proteins

28
Q

An example of glycoprotein

A

. Fibrillin-1

29
Q

What happen if there is a mutation in . Fibrillin-1?

A

Marfan syndrome

30
Q

Components of the basement membrane

A
  1. Type IV. collagen
  2. Proteoglycanes (perlecan)
  3. Adhesive glycoproteins
31
Q

3 examples of Adhesive glycoproteins

A
  1. Laminin-1
  2. Nidogen
  3. Fibronectin
32
Q

3 types of Epidermolysis bullosa

A
  1. Epidermolysis bullosa simplex (intraepidermal epithelial detachment)
  2. Junctional epidermolysis bullosa (lamina lucida detachment)
  3. Dystrophic epidermolysis bullosa (sub-lamina densa detachment)
33
Q

2 enzymes that involve in ECM remodeling

A
  1. Matrix metalloproteinases (MMP)
  2. Tissue inhibitors of metalloproteinases (TIMP)
34
Q

Characteristics of Matrix metalloproteinases (MMP)

A
  1. Zn2+ dependent endopeptidases
  2. Solubile or transmembrane types
35
Q

Characteristics of Tissue inhibitors of metalloproteinases (TIMP)

A
  1. MMP:TMP = 1:1
  2. e.g. alpha-2-macroglobulin, RECK
36
Q

Structure of matrix metalloproteinases

A

Common “minimal domain”:
- Signal sequence
- Prodomain
- Catalytic domain

37
Q

Activation of matrix metalloproteinases

A
38
Q

MMPs’ role in metastasis formation

A
  1. tumour formation, angiogenesis
  2. local invasion
  3. intravasation
  4. transport into circulation, adhesion in small vessels
  5. extravasation
  6. metastasis fomation and angiogenesis (colonisation)
39
Q

Tumour and stroma
-> Cancer-associated fibroblasts (CAF) are formed in the presence of

A
  1. Growth factors: TGF-b, PDGF
  2. Inflammatory citokines: IL-6, IL-10, TNFa
  3. Originated from: tumour cells, fibrocyte, endothel, pericyte, adipocyte…
40
Q

What is the Impact of cancer-associated fibroblasts (CAF)?

A
  1. Further growth of tumour cells
  2. Angiogenesis (VEGF)
  3. ECM remodeling
  4. Immune suppression
41
Q

3 cell adhesion molecules in cell-cell connections

A
  1. Cadherins
  2. Immunglobulins
  3. Selectins
42
Q

An example of cell adhesion molecules in cell-ECM connections

A

Integrins

43
Q

Name 7 Activators of Tumour angiogenesis

A

1/ VEGF
2/ PDGF
3/ HIF-1
4/ TGF-b
5/ FGFs
6/ Angiopoetin 1
7/ MMP

44
Q

Name 4 inhibitors of Tumour angiogenesis

A

1/ TIMP
2/ Thrombospondin
3/ Angiostatin
4/ Thrombostatin

45
Q

4 steps of Wound healing and tissue regeneration

A
  1. Haemostasis (1-2. day)
  2. Inflammatory phase (1-2. day)
  3. Proliferation phase (2-10. day)
  4. Remodeling (1-12. month)
46
Q

What do Throbocytes produce?

A

chemokins, PDGF, TGF-beta

47
Q

Throbocytes produce: chemokins, PDGF, TGF-beta
-> The role of these molecules

A
  1. Leukocyta activation
  2. Fibroblast activation
48
Q

Myofibroblasts – mechano-regulation
-> Identify

A
49
Q

What does it mean if there is an Insufficient wound healing

A

When myofibroblasts do not die in apoptosis
-> May cause Hypertrophic scar and Keloid

50
Q

What is Fibrosis?

A

Pathologic tissue regeneration

51
Q

Where can fibrosis be present?

A
  1. Liver (cirrhosis)
  2. Kidneys
  3. Lungs
  4. Restenosis after PTA
    etc.

Biochem 2 (38 decks)

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