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PATH30001 - Mechanisms of Disease > Lecture 7 - Healing 1 > Flashcards

Lecture 7 - Healing 1 Flashcards

1
Q

Which process is vital for resolution and healing?

A

Turning off of acute inflammation

Removal of the injurious stimulus

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2
Q

Describe the various cell populations in normal homeostasis

A
  • Stem cells
  • Baseline cell population
  • Proliferating cells
  • Differentiated cells
  • Apoptotic cells
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3
Q

How do cells know whether to proliferate or undergo apoptosis?

A

Signalling
• Autocrine
• Paracrine
• Endocrine

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4
Q

What are the different groups of cells in terms of proliferative capacity?

A
  • Labile cells
  • Stable cells
  • Permanent
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5
Q

What are stable cells?

Give some examples

A
  • In G0 phase
  • Can re-enter the cell cycle when exposed to particular stimuli

For example:
• Liver
• Pancreas
• Kidney

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6
Q

What are permanent cells?

Give some examples

A

Non dividing, can never re-enter the cell cycle
eg.
• Neurons
• Myocardium

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7
Q

What are labile cells?

Give some examples

A

Constantly dividing

• Epithelia

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8
Q

What does regeneration require?

What does replacement require?

A

Regeneration:
• Basement membrane
• Extracellular matrix interaction

Replacement:
• ECM interaction

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9
Q

Which cell types are important in healing?

A
  • Fibroblasts
  • Endothelial cells
  • Epithelial cells
  • Osteoblasts
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10
Q

Which ligands are important in proliferation?

A
  • Growth factors
  • Maxtrix proteins
  • Cytokines
  • Hormones
  • Chemokines
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11
Q

Which receptors are important in proliferation?

A
  • Receptor tyrosine kinases
  • GPCR
  • Cytokine receptors
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12
Q

Why is balance between stimulatory and inhibitory signals in proliferation important?

A

Stimulatory required to ‘re-awaken’ cells

However, inhibitory needed to prevent excessive proliferation and cancer

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13
Q

How do receptors without intrinsic catalytic activity function?
Which receptors don’t have intrinsic catalytic function?

A

They interact with a second messenger which does have catalytic activity

Cytokine receptors don’t have intrinsic catalytic activity

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14
Q

Which ligands commonly bind to GPCRs?

A
  • Chemokines

* Hormones

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15
Q

What is the structure of GPCRs?

A

7 transmembrane domains

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16
Q

Describe the activity of RTKs

A
  1. Ligand (often GFs) binds
  2. Dimerisation
  3. Auto-phosphorylation at tyrosine residues
  4. Activation of tyrosine kinase activity
  5. Activation of adaptor molecules

→ Proliferation

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17
Q

Which general processes are brought about by growth factors?

A
  • Proliferation
  • Cell migration
  • Promotion of cell survival
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18
Q

To which receptors do GFs mostly bind?

A

Receptor tyrosine kinases

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19
Q

Describe an example of proliferation without GFs

A
  • Once cells fill out a space, they sense this and stop proliferating
  • Some cells are removed → loss of cell-cell contacts
  • Proliferation triggered
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20
Q

What is EGF?

A

Epithelial GF

• mitogenic for epithelial cells and fibroblasts

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21
Q

What is FGF?

A

Fibroblast GF

• angiogenesis

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22
Q

What is HGF?

A

Hepatocyte GF

• mitogenic for epithelial cells

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23
Q

What is VEGF?

A

Vascular endothelial GF

• vital for growth and proliferation of blood vessels

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24
Q

Which major pathways are involved in growth and proliferation?

A
  • MAPK
  • cAMP
  • JAK / STAT
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25
Describe the sequence of events in the MAPK pathway
1. GF ligand 2. RTK (receptor tyrosine kinase) 3. SOS 4. Ras 5. Raf 6. Mek 7. Erk 8. Gene transcription → proliferation
26
What is the major target of 2° messenger pathways?
Transcription factors
27
What are transcription factors? | Describe their function
Molecules with DNA binding domains | → activation or repression of gene transcription
28
What are some growth promoting transcription factors? | What are these also known as?
* c-fos * c-jun * c-myc Also known as Proto-oncogenes
29
What are some important Tumour suppressor genes?
* p53 * Rb (retinoblastoma protein) * PTEN
30
What is the function of PTEN?
Inhibit growth promoting pathways
31
What are some functions of TGF-β?
NB Pleiotropic: multiple functions * Decreased proliferation (stalls S phase) * Increased collagen production * anti-inflammatory
32
What are the phases of the cell cycle?
``` ( • G0) • G1 • S • G2 • Mitosis ```
33
Why is the cell cycle tightly controlled?
There are many events occurring, and these must occur in a precise order
34
Why is the cell cycle 'cell autonomous'?
These means that within a tissue, each cell has its own time scale for the cell cycle
35
What happens when there is loss of cell cycle control?
• Multi-nucleation | → Cancer
36
What are the phases of mitosis?
* Prophase * Prometaphase * Metaphase * Anaphase * Telophase
37
At which two points is the cell cycle most tightly regulated?
Two checkpoints: • G1 / S checkpoint • G2 / M checkpoint
38
What is being checked at the G2 / M checkpoint?
Proper DNA replication
39
What is being checked at the G1 / S checkpoint?
Errors in DNA
40
Which factors control the cell cycle?
1. Cyclins & CDKs (cyclin dependent kinases) | 2. Cell cycle checkpoints
41
What are the different types of cyclins? | Describe their presence
• Cyclin A • Cyclin B • Cyclin D • Cyclin E The individual concentrations of each rise and fall throughout the cell cycle. This dictates the start and stop of each particular stage
42
Which organs can regenerate? | Why?
Liver • hepatocytes are stable • after partial hepatectomy the hepatocytes re-enter the cell cycle and proliferate to regrow the organ
43
What are the portal triads in the liver?
* Hepatic artery * Hepatic portal vein * Bile duct
44
Describe the process of regeneration in the liver after injury with and w/o damage to the ECM
Injury to cells; ECM intact • full regeneration from residual cells Injury to cells & ECM • disordered deposition of collagen a regeneration from residual cells
45
What happens in Rat corneas when ECM is destroyed
Can't develop properly
46
Compare and contrast the different modes of cell signalling, and give examples of processes that use each
Autocrine: • molecules released by a cell which bind to receptors on that same cell • e.g. liver regeneration Paracrine • molecules released by cells which act on receptors on neighbouring cells • e.g. wound healing Endocrine: • molecules released into the blood stream, which act on target cells far away • e.g. hormones
47
Compare normal and abnormal healing in the skin
``` Normal: • wounds • burns Abnormal: • ulceration • pressure ```
48
Compare normal and abnormal healing in the lungs
Normal: • normal acute healing Abnormal: • ARDS • COPD
49
What happens when 'permanent cells' are irreversibly injured?
Scar; replacement with non-functional tissue
50
Compare Regeneration and Replacement in the healing
Regeneration: • damaged cells replaced with new cells of the same type Replacement: • damaged cells replaced with non functional fibrous tissue
51
Why does the outcome of healing vary?
* different cell types have different regeneration capacities * depending on severity of injury * whether ECM / basement membrane is intact
52
What is the 'dogma' of the molecular mechanisms of healing?
1. Ligand-receptor interaction 2. Second messenger 3. Transcription factor activation 4. Gene expression → action
53
Describe the generalised mechanism of cytokine signalling
1. Cytokine binds cytokine receptor (receptor has no intrinsic catalytic function) 2. JAK / STAT pathway induced 3. Transcription factor activation
54
Which pathway does GPCR activation generally trigger? | Compare this with cytokine receptors.
GPCR: cAMP | Cytokine receptors: JAK / STAT
55
Which general processes are activated by JAK / STAT & cAMP pathways?
* migration * synthesis * secretion or inhibition of these processes
56
What is PDGF?
Platelet derived GF • migration and proliferation of fibroblasts • pro-inflammatory
57
What is the general outcome of the MAPK pathway?
Proliferation
58
What is the ECM?
Extra-cellular matrix • Gel-like meshwork of large proteins ground substance • Structural support for cells • Involved in signalling
59
What are the five stages of the healing process?
1. Demolition 2. Proliferation 3. Migration 4. Synthesis 5. Remodelling
60
Compare the cellular outcomes of: • MAPK • JAK/STAT • cAMP pathway
MAPK: • Proliferation JAK/STAT • Synthesis • Secretion • Migration cAMP: • Synthesis • Secretion • Migration
61
What are 5 important GFs, and what are their respective functions?
1. EGF (TGF) • Mitogenic for epithelium & fibroblasts 2. FGF • Angiogenesis • Migration of macrophages & fibroblasts during wound repair 3. VEGF • Angiogenesis 4. PDGF • Pro-inflammatory • Migration & proliferation of cells 5. HGF • Mitogenic for epithelial cells
62
Describe how cyclins control the cell cycle
1. Specific cyclin expression up regulated 2. Cyclin binds to CDK 3. Cyclin/CDK complex phosphorylates Rb 4. Rb cannot block the cell cycle

PATH30001 - Mechanisms of Disease (34 decks)

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