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Cell Biology > Cell Adhesion and the Extracellular Matrix > Flashcards

Cell Adhesion and the Extracellular Matrix Flashcards

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1
Q

What are GAGs?

A

Glycosaminoglycans

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2
Q

When organised by specific proteins, what do GAGs produce?

A

Glycosaminoglycans, when organised by special proteins, produce proteoglycans

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3
Q

What six types of cells are usually found in connective tissue?

A 
1- Fibroblasts
2- Myofibroblasts
3- Chondroblasts
4- Osteoblasts
5- Adipocytes
6- Blood cells
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4
Q

What are the two main components of ECM?

A

1- Fibrillar proteins

2- Polysaccharide glycosaminoglycans (GAGs) which form proteoglycans

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5
Q

What are four examples of fibrillar proteins?

A

1- Collagen
2- Elastin
3- Fibronectin
4- Laminin

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6
Q

What is the role of fibroblasts?

A

Synthesise collagen, elastin and proteoglycans

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7
Q

Where is collagen synthesised?

A

RER of fibroblast

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8
Q

What is the precursor to collagen?

A

Precollagen then tropocollagen

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9
Q

What does collagen need to form a triple helix?

A

1- Vitamin C

2- Supplied -OH in order to allow for triple helix to form

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10
Q

How is precollagen made into tropocollagen?

A

Precollagen is released into the ECM and cleaved to form tropocollagen. Extremely insoluble.

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11
Q

What is the solubility of tropocollagen?

A

Extremely insoluble

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12
Q

How is tropocollagen made into collagen?

A

Aggregation of tropocollagen via enzyme-catalysed cross-linking, making a fibril

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13
Q

Describe the process of collagen secretion.

A

1- Collagen is packaged into large, specialised vesicles in the RER
2- Collagen secretion occurs by exocytosis at specialised sites
3- Collagen is organised and collagen fibrin is produced in a membrane tube called fibripositor

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14
Q

In regards to surrounding tendons, how are fibroblasts oriented?

A

They are oriented along tendon direction in groups so that collagen produced is correctly oriented (parallelism of tendon)

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15
Q

Where is elastin produced?

A

1- Fibroblasts
2- Smooth muscle cells
3- Chondroblasts

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16
Q

Where is elastin usually found?

A

In places it needs to stretch, e.g. aorta, as it has a tendency to stretch and recoil

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17
Q

What are proteoglycans an assemblage of?

A

GAGs and proteins

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18
Q

What are the roles of proteoglycans?

A

1- Matrix support, cushioning and hydration
2- Glue-like function for adhesion
3- Links between ECM proteins, ECM and cell surgace

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19
Q

Describe the structure of GAGs.

A

1- Long chains of repeating disaccharide units
2- Highly negatively charged
3- Highly hydrated

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20
Q

What is hyalyuronic acid?

A

A repeating dissacharide in GAG

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21
Q

How is ECM linked to cytoskeleton?

A

1- Collagen or proteoglycan

2- These bind fibroconectin, which links to integrins, which in turn bind via adatorss to the actin cytoskeleton

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22
Q

What are the roles of myofibroblasts?

A

1- Secrete collagen (fibroblast-like)

2- Synthesise actin, myosin and desmin (smooth-muscle like)

23
Q

What do granules in mast cells contain?

A

1- Heparin

2- Histamine

24
Q

How are myofibroblasts involved in tissue damage?

A

1- Prolerate
2- Secrete collagen which helps form a scaffold
3- Consolidate damaged area by forming a fibrous scar
4- Contract to reduce the size of damaged area, thus expressing focal adhesions and smooth muscle actin

25
Q

What is the main role of plasma cells?

A

Producing antibodies through the secretory pathway

26
Q

What is the main role of macrophages?

A

Ingesting Listeria bacteria/paramecium

27
Q

What are the main roles of adipocytes?

A

1- Insulation
2- Packing
3- Storing energy

28
Q

What is the ob gene?

A

1- Mutant gene
2- Leads to excessive eating
3- Obesity is induced
4- ‘Deleted’ by leptin

29
Q

What provides the satiety signal?

A

Leptin

30
Q

What happens to leptin levels in obese patients?

A

Increases due to decreased sensitivity/increased resistance

31
Q

What are the roles of tight junctions?

A

1- Define polarity
2- Control passage of substances between cells
3- Link to actin cytoskeleton

32
Q

What is the role of tight junctions?

A

Plaque anchors actin filaments at the membrane

33
Q

What are the four main types of cadherins?

A

1- E-cadherin
2- N-cadherin
3- P-cadherin
4- VE-cadherin

34
Q

Where are E-cadherins usually found

A

Epithelia

35
Q

Where are N-cadherins usually found?

A

1- Neurons

2- Heart muscle

36
Q

Where are P-cadherins usually found?

A

1- Placenta

2- Epidermis

37
Q

Where are VE-cadherins usually found?

A

Endothelial cells

38
Q

What is the role of desmosomes?

A

Linking between strong intermediate filaments and adjacent cells

39
Q

What are the two main structural components of desmosomes?

A

1- Plaque

2- Filaments

40
Q

What are the roles of gap junctions?

A

1- Communication
2- Hydrophobic channel
3- Allow passage of small molecules
4- Coordinate function

41
Q

What are the roles of focal adhesions?

A

1- Link ECM with cell cytoskeleton
2- Ac as signalling platforms
3- Link to fibronectin

42
Q

How do focal adhesions link the ECM with cell cytoskeletons?

A

Link ECM through integrins with actin filaments of the cytoskeleton

43
Q

What are the roles of hemidesmosomes?

A

1- Link ECM to cell cytoskeleton

2- Link to laminin in basement membrane

44
Q

How do hemidesmosomes link the ECM with cell cytoskeletons?

A

Link ECM though integrins to intermediate filaments of cytoskeleton

45
Q

What are integrins?

A

Large family of proteins which bridge between the cell cytosol and ECM

46
Q

Give two examples of integrins.

A

1- Fibronectin

2- Laminin

47
Q

What is Duchenne’s Muscular Dystrophy?

A 
1- A gene mutation which leads to the absence of dystrophin (adaptor) due to the premature termination of translation
2- Leads to damage to muscle fibre
3- Muscle wasting
4- Muscle weakness
5- Unable to walk by 12 years of age
48
Q

What is the cause of Duchenne’s Muscular Dystrophy?

A

Gene mutation which leads to the absence of dystrophin (adaptor) due to the premature termination of translation

49
Q

What is PTC 124?

A

1- Also called ataluren
2- Experimental druh
3- May override premature stop signal mutation and lead to normal production of dystrophin

50
Q

What are the three steps of cell adhesion in cancer stages?

A

1- Carcinoma in situ
2- Microinvasion
3- Progression to metastasis

51
Q

Define carcinoma in situ.

A

1- Tumour cells accumulate to cells’ mutations disregulating the normal cell cycle
2- Cells have yet not breached basement membrane

52
Q

What happens during microinvasion?

A

1- Expression of cadherins is reduced, leading to the cells converting to ‘mesenchymal’ cells
2- Microinvasion begins and is aided by the secretion of metalloproteases
3- Basement membrane is breached
4- In invading tumours, cells express integrin to promote interaction with ECM and non-epithelial cells during movement

53
Q

What happens in progression to metastasis?

A

1- Autocrine motility factors are secreted thus increasing motility
2- Angiogenesis factors such as VEGFs are secreted thus promoting vascularisation
3- Metastising tumour enters into lymphatic and blood circulations
4- Invasive carcinoma

Cell Biology (20 decks)

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