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Semester 2 Molecular Medicine > Lipids and cell membranes > Flashcards

Lipids and cell membranes Flashcards

1
Q

What are the 6 steps of cell to cell communication?

A
  1. Synthesis of signal
  2. Release of the signalling molecule by the signalling cell
  3. Transport of the signal to the target
  4. Detection of the signal by a specific receptor protein
  5. A change in cellular metabolism, function or development triggered by the receptor- signal complex
  6. Removal of the signal or desensitisation
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2
Q

What are the 2 long range transport of signal methods?

A
  • Endocrine

* Neurotransmission

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3
Q

What is endocrine transport?

A

The hormone is released by an endocrine cell and is carried in the bloodstream to distal target cells

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4
Q

What is an example of endocrine transport?

A

Follicle stimulating hormone released form the pituitary acts upon the ovary

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5
Q

Give an example of neurotransmission

A

Breathing- the phrenic. and thoracic nerves send impulses from the brain to the diaphragm

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6
Q

What is paracrine signalling?

A

Signalling molecules that only affect target cells in close proximity to secreting cells

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7
Q

Give an example of paracrine signalling

A

Somatostatin release by pancreas cells acts locally (Neurotransmission can also be considered a type of paracrine signalling)

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8
Q

What is autocrine signalling?

A

Cells respond to substance that they themselves release

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9
Q

Give an example of autocrine signalling

A

Some neurotransmitters and growth factors bind to the cells that release them (lets cells know that enough has been released)

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10
Q

What are the short range signalling methods

A
  • Paracrine signalling
  • Autocrine signalling
  • Membrane bound proteins that intact to signal (T cells)
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11
Q

Give an example of a type of cell in which multiple types of signalling can be occurring simultaneously and describe how

A
  • Insulin release from pancreatic beta cells
  • Autocrine
  • Paracrine to alpha cells
  • Endocrine: insulin enters the blood stream where it travels to the liver /muscle/ Adipose Tissue
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12
Q

What are the 4 types of receptor?

A
  1. Ligand gated ion channels (ionotropic receptor)
  2. G-protein-coupled receptors (metabotropic)
  3. Kinase-linked receptor
  4. Nuclear receptor
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13
Q

Describe the ligand gated ion channel receptor including time frame and an example

A

Binding opens an ion channel which leads to hyper polarisation or depolarisation of the cell
• Milliseconds
• Nicotinic acetylcholine receptor

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14
Q

Describe the G-protein-coupled receptors including time frame and an example

A

Binding activates a G protein which then goes on to either:
• Open a ion channel, causing the cell to become hyper polarised or depolarised
• Activate a second messenger pathway causing calcium release, protein phosphorylation or something else which causes a cellular effect
• Seconds
• Muscarinic Acetylcholine receptor

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15
Q

Describe the Kinase-linked receptor including time frame and an example

A
  • Binding causes protein phosphorylation which causes gene transcription then protein synthesis
  • Hours
  • Cytokine receptors
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16
Q

Describe the nuclear receptor including time frame and an example

A
  • Signalling molecule enters the cell and then the nucleus where it binds to the receptor
  • Binding in the nucleus causes gene transcription and then protein synthesis
  • Hours
  • Oestrogen receptor
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17
Q

What are eicosanoids?

A

They are inflammatory mediators known as local hormones
• They have specific effects on target cells close to their site of formation
• They are rapidly degraded(not transported to the distal sites within the body
• Main source is arachidonic acid

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18
Q

What are the principle eicosanoids?

A
  • Prostaglandins
  • Thromboxanes
  • Leukotrienes
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19
Q

Describe the structure of arachidonic acid

A
  • 20 carbon unsaturated fatty acid

* contains 4 double bonds

20
Q

What is the effect of prostaglandins?

A
  • Dependent on the receptor: EP1=vasoconstriction, EP2= vasodilation
  • Involved in the inflammatory response, thermoregulation (fever) and pain
21
Q

Where are prostaglandins synthesised?

A

In all tissues and cell types

22
Q

What is Phophatidylinositol?

A
  • Phosphatidylinositol 4,5-bisphosphate (PIP2) is a phospholipid in the lipid bilayer
  • It is the substrate of phospholipase C (PLC)
  • PLC liberates 2 signalling molecules from PIP2: Inositol 1,4,5 trisphosphate (IP3) and diacyglycerol (DAG)
23
Q

Describe the Inositol phospholipid signalling pathway

A
  • Signalling molecule binds to a G protein linked receptor
  • G protein alpha subunit is activated and activate phospholipase C (PLC)
  • Phospolipase liberates 2 signalling molecules from PIP2: Inositol 1,4,5 trisphosphate (IP3) and diacyglycerol (DAG)
  • The IP3 causes Ca2+ channels in the endoplasmic reticulum to open
  • PKC is activated
24
Q

Give 3 substrates for PKCs

A
  1. Tumour supressor p53 which prevents tumour formation
  2. Ca v 1.2 (a calcium channel) which causes heart contraction
  3. IKKα (cytokine) which activates B cells
25
Q

What happens to IP3 after signal transduction has taken place?

A

IP3 is recycled back to the membrane as PIP2

26
Q

What are thromboxanes?

A
  • Synthesised in platelets
  • Short lived (autocrine/paracrine)
  • Thromboxane A2 (TXA2) has prothrombotic properties
  • Stimulate platelet aggregation
  • Vasoconstrictor
27
Q

What are leukotrienes?

A
  • Synthesised in white blood cells (Leuko)
  • Contain a triene system of double bonds
  • Some contain cysteine
  • Involved in the immune response
  • Heavily implicated in asthma and allergy
28
Q

What is involved in vasoconstriction?

A
  • Thomboxanes
  • Prostaglandins (EP1 receptor)
  • Platelet activating factor
29
Q

What is involved in vasodilation?

A

• Prostaglandins (EP2 receptor)

30
Q

What stimulates platelet aggregation?

A
  • Thromboxane
  • Platelet activating factor
  • Prostaglandins can both inhibit and promote it
31
Q

What is involved in inflammation?

A
  • Platelet activating factor

* Prostaglandins

32
Q

What is involved in the immune response?

A
  • Leukotrienes

* Platelet activating factor

33
Q

What are NSAIDs?

A
  • Non steroidal anti-inflammatory drugs

* e.g. Aspirin and Ibuprofen

34
Q

What is the affect of NSAIDs?

A
  • Inhibit the formation of prostaglandins involved in fever, pain and inflammation
  • Inhibit blood clotting by blocking thromboxane formation in blood platelets
35
Q

What is the mechanism of action of ibuprofen?

A

• Block the hydrophobic channel by which arachidonate enters the cyclooxygenase active site

36
Q

What is the mechanism of action of aspirin?

A
  • Inhibits thromboxane formation via COX-1 inhibition in blood platelets
  • Acetylates a serine hydroxyl group near the active site, preventing arachidonate from binding
  • Aspirin binds irreversibly
37
Q

why are the effects of aspirin long lived?

A

Because platelets lack a nucleus and don’t make new enzymes

38
Q

How is arachidonic acid formed?

A

From Phospholipids via chemical and mechanical stimuli which activate PLA2

39
Q

How can Arachidonic acid be metabolised?

A

a) By cyclo-oxygenase and peroxidase
• Produces endoperoxidases
b) By lipoxygenases to give leukotrienes

40
Q

What is formed from Endoperoxidases?

A
  • Prostaglandins
  • Prostacyclin
  • Thromboxane A2
41
Q

How is Platelet Activating factor formed?

A

From Phospholipids (PLA2 enzyme)

42
Q

How are prostaglandins formed?

A
  • Phospholipid –> Arachidonic acid (PLA2)
  • Arachidonic acid –> Endoperoxidases (Cyclooxygenase)
  • Endoperoxidases –> Prostaglandins
43
Q

What are some examples of lipid soluble molecules?

A
  • Cortisol
  • Estradiol
  • Testosterone
  • Thyroxine
44
Q

Describe the mechanism of action of cortisol

A
  • Passes into the cell
  • Binds to an intracellular receptor protein which becomes activated
  • The activated receptor-cortisol complex moves into the nucleus
  • The complex binds to the regulatory region of the target gene and activates transcription
45
Q

Describe the formation of eicosanoids

A
  • Phospholipids to arachidonic acid and platelet activating factor (PAF) by action of Phospholipase A2 (PLA2)
  • Arachidonic acid to endoperoxidases by action of cyclooxygenases and peroxidase
  • Arachidonic acid to hydroperoxy and hydroxy fatty acids by action of lipoxygenase
  • Endoperoxidases to prostaglandins, prostacyclin and thromboxane A2
  • Hydroperoxy and hydroxy fatty acids to leukotrienes

Semester 2 Molecular Medicine (27 decks)

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