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BSMS 102 > Theme 3 - intercellular signalling > Flashcards

Theme 3 - intercellular signalling Flashcards

1
Q

what is intercellular signalling?

A

extracellular signalling between cells

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2
Q

what is intracellular signalling?

A

occurs within cells

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3
Q

give four reasons why cells need to communicate

A

communicate with neighbour cells, adapt metabolism and nutritional requirements to nutritional state of the body, induce or stop growth/cell division, respond to danger signals

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4
Q

what can bone marrow stem cells become?

A

all components of the blood

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5
Q

when new cells are needed, what must stem cells do?

A

upregulate proliferation by the right amount and differentiate to the desired cell type

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6
Q

what are the five basic steps of intercellular signalling?

A

synthesis and release of the signal molecule, transport of signal molecule to target cell, detection of the signal by a receptor on the target cell, change in cellular behaviour due to activated of the receptor, removal of the signal

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7
Q

two ways a signal can be removed to terminate cellular response?

A

removal of ligand binding the target receptor or removal of the receptor itself

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8
Q

name four types intercellular signals with examples

A

proteins (Interferon and insulin), peptides (glucagon and growth hormone), small chemicals (steroids made from cholesterol and amino acid metabolites), dissolved gases (nitric oxide)

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9
Q

name two steroids made from cholesterol that can be used as intercellular signals

A

estradiol and cortisol

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10
Q

name two amino acid metabolites that can be used as intercellular signals

A

adrenaline and histamine

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11
Q

what three factors must be in place for a cell to respond to a signal?

A

ligand present, responding cell has relevant receptor, receptor is correctly coupled to an intracellular signalling pathway

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12
Q

what determines what receptors are present on a cell and to what level they are expressed?

A

gene expression and levels can be determined by the cellular environment

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13
Q

give two reasons why a cell may not respond to a signal even though it has the correct receptor?

A

the cell may have already been exposed to the signal or there may be an interacting signal that affects the receptor activity

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14
Q

why are most receptors found at the cell surface?

A

many signalling molecules cant cross the lipid membrane as they are too large or too hydrophilic

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15
Q

what are the three main types of receptor?

A

ion channels. GPCRs and enzyme linked receptors

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16
Q

what are three effects of receptor activation and how long do they take?

A

altered protein function eg contraction (seconds), secretion (mins), protein synthesis (12-24 hours)

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17
Q

what two classes of molecule can pass the cell membrane and bind intracellular receptors?

A

small molecules (nitric oxide) and hydrophobic molecules (steroid hormones and thyroxin)

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18
Q

what type of receptors are found intracellularly?

A

nuclear receptors - whole ligand receptor complex moves to the nucleus to exert its effects

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19
Q

what happens to a cell if it is not receiving any signals?

A

it will undergo apoptosis

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20
Q

give an example of two cells responding differently to the same molecule

A

adrenaline - causes smooth muscle contraction in gut blood vessels but relaxation in blood vessels of smooth muscle cells supplying muscles

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21
Q

why can one molecule (adrenaline) exert different effects on different tissues?

A

presence of different adrenergic receptors - alpha adrenergic in the gut causing contraction and beta adrenergic in the skeletal muscle to cause relaxation

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22
Q

what receptors does adrenaline bind to in the gut and what does this cause?

A

binds to alpha adrenergic receptors and this causes contraction

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23
Q

what receptors does adrenaline bind to in the skeletal muscle and what does this cause?

A

binds to beta adrenergic receptors and this causes relaxation

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24
Q

what type of receptors are adrenergic receptors?

A

GPCRs

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25
Q

what ligand binds to muscarinic M1 and M2 receptors?

A

acetylcholine

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26
Q

what type of muscarinic receptors does Ach bind on salivary glands and what is the effect?

A

Ach binds M1 muscarinic receptors in the salivary glands and this causes secretion

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27
Q

what type of muscarinic receptors does Ach bind on heart pacemaker cells and what is the effect?

A

Ach binds the M2 muscarinic receptors in the heart and causes decreased rate of firing

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28
Q

what ion channel can Ach activate and where is this found?

A

Ach can activate nicotinic receptors eg Na+/K+ ATPase on skeletal muscle

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29
Q

what effect does Ach have on skeletal muscle

A

contraction via binding to nicotinic sodium potassium ATPase

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30
Q

how can one signal have many different effects?

A

depends on what receptors are present and what signalling pathways they activate

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31
Q

name a long range (m) signal

A

endocrine

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32
Q

name four short range (micrometer) signals

A

paracrine, neuronal, autocrine and juxtacrine

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33
Q

how does a hormone exert its effects?

A

released from an endocrine gland into the bloodstream, bathes all body cells in the hormone but only some cells have the right receptor to respond - usually affect gene expression

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34
Q

what happens when you eat food and blood sugar increases?

A

beta cells in IOL in the pancreases recognise increase in blood glucose and releases insulin

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35
Q

what does insulin do when released due to increased blood glucose?

A

activates liver cells, skeletal muscle and adipocytes to take up the excess glucose

36
Q

what cells take up excess glucose?

A

liver cells, skeletal muscle cells and adipocytes

37
Q

what cell types sense when blood glucose is too low and how do they respond?

A

alpha cells in the IOL of the pancreas respond by releasing glucagon

38
Q

what does glucagon do?

A

released when blood glucose is too low and signals to the liver and adipocytes to release glucose

39
Q

what can signalling errors result in?

A

type I or type II diabetes

40
Q

what happens in type I diabetes

A

autoimmune and early onset - immune system destroys beta cells in IOL so insulin isn’t made

41
Q

what happens in type II diabetes

A

absent or decreased response to insulin by liver cells and adipocytes

42
Q

name one way glucose levels can be controlled in type II diabetes

A

with diet

43
Q

what receptor does cortisol bind and where is it found?

A

binds the glucocorticoid receptor which is found intracellularly

44
Q

what effects can the cortisol-GC receptor complex have on gene expression?

A

acts as a transcription factor to activate or suppress gene expression

45
Q

name two effects of cortisol

A

drive production of glucose or be anti-inflammatory by regulating T cells

46
Q

name three synthetic hormone drugs that activate the glucocorticoid receptor

A

hydrocortisone, prenisolone, dexmethasone

47
Q

name three conditions where synthetic steroids can be used as drugs

A

autoimmune - psoriasis/ulcerative colitis, allergy - urticaria and asthma

48
Q

what drug can be given in asthma

A

dexmethasone

49
Q

what is paracrine signalling?

A

release of signalling molecules that diffuse locally to neighbour cells only

50
Q

name three types of molecule that can be paracrine signals

A

proteins, amino acid derivatives and dissolved gases (NO)

51
Q

name two proteins that act in a paracrine manner

A

cytokines (immune response) or platelet derived growth factor (stimulates cell proliferation)

52
Q

name an amino acid derivative that acts in a paracrine manner

A

histamine - released from mast cells and induces local inflammation - derivative of histidine

53
Q

what amino acid is nitric oxide a derivative of and what effects does it have

A

Argenine and it causes vasodilation by relaxing smooth muscle

54
Q

how is NO made from argenine?

A

act activates IP3 in endothelial cells in blood vessels which causes calcium release which activates NO synthase and argenine makes NO

55
Q

what is target enzyme does NO bind to and where is this found?

A

guanylate cyclase and is found in the cytoplasm

56
Q

what does guanylate cyclase do once bound to NO?

A

converts GTP to cGMP and relaxes smooth muscle and increases blood flow through the vessel

57
Q

how long is the half life of cGMP and why?

A

short half life (10 seconds) as it is quickly hydrolysed by phosphodiesterase

58
Q

how does PDE hydrolyse cGMP?

A

cleaves the cyclic bond

59
Q

where can interfering with PDE be clinically useful and why?

A

cardiovascular disease - use a small molecule to inhibit PDE and therefore increase the half life of NO leading to prolonged smooth muscle relaxation

60
Q

what other effect was the PDE inhibitor developed by Pfizer found to have besides in CAD?

A

anti impotence

61
Q

what drugs target PDE 5 and where is it expressed?

A

viagra - PDE 5 is expressed in the corpus caveosum

62
Q

what would inhibiting PDE do to cAMP?

A

increase its half life by preventing its hydrolysis

63
Q

give one clinical use of NO

A

treatment of angina (nitroglycerin)

64
Q

what are the symptoms of angina?

A

pain radiating down the left arm due to decreased blood flow to the heart

65
Q

how does nitroglycerin treat angina?

A

nitroglycerin tablet or patch is quickly converted to NO which leads to vasodilation and therefore increased blood flow to coronary arteries

66
Q

what type of paracrine signalling only happens at NMJs?

A

neuronal signalling

67
Q

what does adrenaline do when acting as a neurotransmitter?

A

regulates attentiveness and mental focus

68
Q

what does adrenaline do when acting as a hormone?

A

redirects blood to the muscles and increases conversion of glycogen to glucose

69
Q

give one example of where Ach can be released

A

in the gut to innervate muscle cells

70
Q

what is serotonin derived from and give an examples of what it is implicated in

A

derived from tryptophan and can modulate mood

71
Q

what is dopamine derived from and give an examples of what it is implicated in

A

derived from tyrosine and involved in fine tuning of motion

72
Q

what is autocrine signalling?

A

when cells secrete signals that bind their own receptors and generate a change in their own behaviour - short distance

73
Q

what kind of feedback loop is autocrine signalling an example of?

A

positive feedback

74
Q

Give an example of a positive feedback loop mediated by autocrine signalling

A

TNF cytokine production from monocytes which feeds back onto the TNF receptors on the cell to amplify the signal and increasing further cytokine production

75
Q

what molecule is implicated in cancer when autocrine signalling goes wrong?

A

EGF - uncontrolled release of EGF by cells which acts on the cells causing it to grow and divide out of control - tumour

76
Q

what is juxtacrine signalling?

A

contact dependent signalling where no signalling molecule is released - happens between immediate neighbours via membrane bound molecules

77
Q

what are two examples of juxtacrine signalling?

A

gap junctions and contact dependent ligand receptor binding

78
Q

how do gap junctions mediate juxtacrine signalling?

A

cells line up and form a channel between them that allows transfer of cytoplasmic contents eg ions, nucleotides and sugars

79
Q

how does contact dependent ligand receptor binding mediate juxtacrine signalling?

A

direct cell communication or interactions with the ECM

80
Q

what causes gap junctions to open or close?

A

phosphorylation

81
Q

what subunits are gap junctions made of and how many of these form a channel?

A

connexons (20 types) and 6 subunits associate to form a connexion channel

82
Q

what governs what can pass through a gap junction?

A

how big the molecule is and which amino acids line the channel (their polarity etc)

83
Q

give two examples of a tissue where gap junctions are found

A

in the heart to allow co-ordinated contraction and in the myometrium to co-ordinate uterine contractions during childbirth

84
Q

give an example of contact dependent ligand receptor binding

A

T cell and antigen presenting cell - T cell recognises a pathogen presented on an MHC II

85
Q

what is the mechanism of contact dependent ligand receptor binding in T cells and APCs?

A

APC engulfs a pathogen and presents it on MHC II, T cell recognises this and becomes primed, co stimulatory CD80 is upergulated on the APC surface, CD80 simultaneously engages with CD28 on T cell and boosts the signal to allow differentiation of the T cell into the relevant T cell

BSMS 102 (14 decks)

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