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psc2002 > lecture 6 > Flashcards

lecture 6 Flashcards

1
Q

what are the two types of Cl- channels?

A

CFTR and Ca2+ activated Cl- channel (CaCC)

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2
Q

what is channel activity regulated by?

A

PKA and ATP

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3
Q

how does the CFTR channel open and close?

A
  1. PKA phosphorylation of RD induces ATP binding and dimerisation of NBDs
  2. conformational change in NBDs terminal transmitted to MSDs- leading to pore opening
  3. ATP hydrolysed and pore closes
  4. dephosphorylation of RD by protein phosphotases closes the channel, even in prescence of ATP
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4
Q

what does CFTR require to open?

A

ATP binding and PKA phosphorylation

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5
Q

where are Calcium activated Cl- channels (CaCC) found?

A

-present in apical membrane of most epithelial cells that express CFTR
-apical Membrane of gland secretory acinar cells
-endocrine cells, smooth & skeletal muscle, neurones

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6
Q

how are CaCC activated?

A

-by rise in cytosolic Ca2+

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7
Q

what regulates CaCC?

A

calmodulin and calmodulin dependent kinase

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8
Q

what is the structure of TMEM16A?

A

-10 TMDs
-pore region is TMD 6-9
-Ca2+ ions bind to glutamate residues in one fo the two alpha helices of intracellular loop 3 (opens pore, enables Cl- transport)

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9
Q

what are the two mechanisms in which HCO3- is secreted?

A
  1. directly through Cl- channel itself
  2. indirectly, via coupling the Cl- channel with an apical Cl-/HCO3- exchanger
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10
Q

what does cAMP/PKA activation in CFTR switch on?

A

anion epithelial activity
-requires physical interaction of 2 proteins aided by scaffold protein CAP70 and CFTR RD phosphorylation

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11
Q

what happens in CF with anion exchangers?

A

-anion exchanger activity is inhibited
-reduces net HCO3-
-reduces fluid secretion

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12
Q

what do acinar cells do?

A

-secrete digestive enzyme
-produce low volume NaCl rich fluid into ducts using TMEM16A channels

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13
Q

what do duct cells do?

A

-transport digestive enzymes to small intestine
-produce high volume NaHCO3 rich secretion using CFTR and SLC26A6

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14
Q

what is the CF treatment?

A

pancreatic enzyme replacement therapy (PERT)

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15
Q

what is fluid secretion driven by?

A

NaCl and NaHCO3- secretion
with CFTR the dominant anion channel

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16
Q

what is fluid absorption driven by?

A

multiple absorptive mechanisms depending on site in GI tract

17
Q

what does failure in fluid absorption or excessive fluid secretion lead to?

A

rapid dehydration, electrolyte imbalance, death

18
Q

where does ENaC mediated fluid absorption occur?

A

-colon

19
Q

what are the other two types of absorption?

A
  1. Na linked absorptive ion transporters (NaCl)
  2. nutrient absorptive transporters
20
Q

what condition occurs with dysregulation of fluid homeostasis?

A

secretory diarrhoeas (SD)

21
Q

what is secretory diarrhoea?

A

-2nd leading cause of death in under 5s
-caused by dysregulation in cell signalling

22
Q

how can SD be prevented?

A

by safe drinking water, adequate hygiene and sanitation

23
Q

what occurs in SD with cholera toxin infection?

A

-cholera toxin inhibits NaCl and fluid absorption
-stimulates CFTR mediated Cl-/HCO3- and fluid secretion

24
Q

how does this infection occur?

A

-cholera toxin causes ADP-ribosylation of G protein that blocks GTP hydrolysis
-anion channel becomes permenantly active- lots of cAMP
-leads to uncontrolled overstimulation of CFTR and inhibits NaCl absorption
= excessive salt and water loss into intestinal lumen = severe diarrhoea

25
Q

what is the treatment for SD?

A

oral rehydration therapy
intravenous fluid

26
Q

what is oral rehydration therapy?

A

-isomolar or hypo-osmolar salt solution containing NaCl, NaCitrate, KCl and glucose

27
Q

why is starch better than using glucose?

A

-starch prolongs action of ORT

28
Q

what does ORT do?

A

causes rapid fluid reabsorption by utilising the nutrient absorptive transporters

psc2002 (15 decks)

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