Epithelial Cells.txt

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Epithelial Cells.txt
2012-10-04 13:32:46
PSL Physiology

Lectures 5-8
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    • author "JLeezy"
    • tags "PSL"
    • description "Lectures 4-8"
    • fileName "Epithelial Cells"
    • freezingBlueDBID -1.0
    • Epithelial Cells
    • Transport and secretory cells
  1. Two sections of epithelial cells
    • Apical: flat side that interacts with lumen
    • Basolateral: rest of the cell's surface, interacts with blood/ECF
  2. Trans- vs. Paracellular
    Transcellular is through cells, paracellular is between them (via tight junctions).
  3. How do the kidneys reabsorb nutrients?
    • Nutrients begin in lumen
    • Na+/K+ pumps create Na+ concentration gradient (Na+ goes out of cells)
    • Na+ gradient powers active transport of nutrients into cells via apical side
    • Nutrients exit cells via passive carrier proteins on basal side
  4. Symptoms of CF
    Thick mucus secretions and salty sweat.
  5. Three hypotheses of how CF causes lung infections
    • 1: A large decrease in Cl- absorption (mutant CFTR) --> increase in NaCl concentration on airway surfaces --> impedes natural antibiotics, leading to more infections
    • 2: A large increase in Na+ absorption (no CFTR, no ENaC inhibition) --> water follows solute --> low airway surfaces liquid volume --> more infections
    • 3: No CFTR-mediated HCO3- transport --> without HCO3- being secreted into the airways, pH gets too acidic (?) or causes a lack of defensins (?) --> more infections
  6. CFTR
    Anion (Cl-) channel. Mutated in CF. Inhibits ENaC channel when working properly.
  7. ENaC
    Na+ channel
  8. Exocrine vs. endocrine secretion
    • Exocrine: secretion into lumen
    • Endocrine: secretion into bloodstream (long-range)
  9. Parotid
    Secretory gland for saliva
  10. How does secretion work?
    Cl- enters cell via basolateral side and exits via apical side (into lumen); water follows solute.
  11. Cellular path of proteins that are destined for secretion
    These proteins are made on the rough ER, sent to the Golgi, then the plasma membrane.
  12. Pulse-Chase experiments (and results)
    • Add labeled amino acids to pancreatic cells for only three minutes to see where proteins that were synthesized during those three minutes go.
    • 3 min: rough ER
    • 10 min: Golgi
    • 30 min: ready for secretion @ membrane
  13. Translocons
    Pores that trap growing polypeptides halfway across the lipid bilayer. Periodically open during the protein's growth to give it a chance to stay in cytosol or head to the membrane.
  14. Coat proteins
    Cover vesicles and help with curvature AKA formation of the vesicles.
  15. SNARES (2 types)
    • Proteins that assist with vesicle fusion.
    • v-SNARES: In the Vesicle, bind to t-SNARES
    • t-SNARES: Extend from vesicle's Target location
  16. Endocrine vs. paracrine agents
    • Endocrine agents, AKA hormones, transmit signals over long distances
    • Paracrine agents affect nearby cells
  17. Dissociation equation (a smaller Kd means. . ?)
    • Kd=[L][R]/[LR]
    • Smaller Kd means more sensitive signal reception.
  18. Agonist vs. antagonist
    • Agonists are ligands that are activators
    • Antagonists are ligands that are inhibitors
  19. nAchR
    Na+ (and some Ca++) channel that requires two Ach molecules to bind for it to open. Nicotine can do the function of Ach.
  20. GPCR: cAMP Pathway
    Ligand binds GPCR --> activates G-protein --> β and γ subunits head off to open a K+ channel and inhibit some Ca++ channels --> α subunit activates/inhibits adenylyl cyclase --> adenylyl cyclase increases/decreases cAMP levels --> 4 cAMP molecules activate PKA complex
  21. GPCR: Ca++ Pathway
    Ligand binds GPCR --> activates G-protein --> β and γ subunits head off to open a K+ channel and inhibit some Ca++ channels --> α subunit activates PLC --> PLC hydrolyzes (splits) PIP2 into IP3 and DAG --> IP3 releases Ca++ from the ER, DAG activates PKC
  22. Calmodulin
    Protein that requires 4 Ca++ molecules to bind. Once activated, calmodulin can binds to and activate other proteins.
  23. Methods of GPCR regulation (@ receptor, G-protein, and second messengers)
    • Receptor: desensitization, down regulation
    • G-protein: GTPase, lipid modification
    • Second messengers: elimination of second messengers from cell
  24. β-adrenergic pathway
    Norepinephrine binds β-receptor --> G-protein, adenylyl cyclase, cAMP, PKA --> PKA phosphorylates SNARES, causing them to fuse and secrete their proteins
  25. How does salivation work?
    IP3 releases Ca++ from the ER. This Ca++ activates Cl- channels and transporters, allowing Cl- to leave the cell. Water follows solute - voila! Salivation!
  26. What causes Cholera?
    Constant activation of G-proteins (and thus adenylyl cyclase --> cAMP --> PKA), and PKA keeps CFTR activated.
  27. Nuclear Receptor Superfamily
    Large class of intracellular receptors that control hormones and nutrients as signals. Each has three sections: activation, DNA binding, and ligand binding.
  28. Ras
    • A simple (just has an α subunit) G-protein that activates MAP kinase.
    • *Some cancers are caused by a mutated Ras that results in continual activation.
  29. MAP kinase
    Regulates the entire cell cycle.
  30. Receptor Tyrosine kinases
    • Once activated (ligands bind) they dimerize, and then activate Ras with the classic GDP --> GTP.
    • *No second messengers in this pathway.