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Lecture

PHSL233 lecture 05.doc

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Department
Physiology
Course
PHSL233
Professor
Kirk Hamilton
Semester
Spring

Description
PHSL233 Lecture 05 Signal transduction in Epithelia II This is signal transduction pathways of a stomach parietal cells which is a specilised epithelial cell. It secretes acidic fluid to stomach to aid with digestion. Secretagons are ligands or stimulatory agonist that will stimulate this pathway to release acid, histamine, acetylcholine and gastrin are the main ones. All agonist are working through GPCR, histamine is working through adenylyl cyclase whereas Ach and gastrin are working through phosphatelipase C, but they all leading to the same acidic secretion effect. The main inhibitory is somatostatin. Histamine Vagal nerve stimulates enteric nerve which stimulates enterochromaffin cells (ECL) to release histamine. Closeby are parietal epithelial cells, histamine act on H2 receptors (GPCR) on the basolateral membrane of the parietal epithelial cell. This activates the alpha-s subunit and in turn adenylyl cyclase is excited causing increase of cAMP and PKA levels. PKA then phosphyorlates a H-K pump making a H-K -P pump. This will cause a increase in acidic H+ to be pumped out of the cell while K is pumped in, thus increase in transport rate. Due to the movement of H+, you will get Cl and water following so ending up with HCl and water being secreted out of the cell into lumen of stomach. Acetylcholine vagal nerve stimulates enteric nerves releasing Ach, Ach can also directly stimulate the release of histamine. Ach bind onto M3 receptor on basolateral membrane (GPCR) of parietal epithelial, note that GPCR always have 7 transmembrane domains. On binding of Ach on the extracellular receptor, this will cause conformational change which change is transferred onto the G protein and thus activating it. Alpha-q activates phosphatelipase C which produce DAG and IP3. This then cause increase of Ca and in turn PKC which phosphorylates H-K pump and causing excretion of HCL into lumenal stomach from parietal epithelial cell. The pancreatic acinar cells secretes enzymes which are essential for digestion, there are also a lot of ligands against stimulating signals with receptors sitting in the basolateral membrane. Resulting in secretion of HCO3 (bicarbonate) rich fluid on the apical surface and into lumen of duct. Ach, gastrin etc are all increasing secretion whereas somatosatatin are inhibiting secretion. Secretin main stimulis of secretin secretion is acid PH in the duodenum increased, acid fluid is secreted in the stomach and enters the intestinal tract in which it must be neutrilised by bicarbonate. So acinar cells of pancreas recognise this low PH, it will secrete secretin which binds onto basolateral membrane of pancreatic duct epithelial cells (M3 GPCR) and activating alpha-s. This in turn activating adenylyl cyclase and increase cAMP and then PKA. PKA then phosphorylates CFTR which is cystic fibrosis transmembrane conductance regulator, mutation in this protein causes cystic fibrosis and it is a Cl channel in pancreas but also transport bicarbonate (HCO3). So CFTR-P is formed, this will start transport of bicarbonate and chloride out into the lumen of duct, pancreatic duct epithelial cell secretes bicaronbate rich fluid into lumen of du
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