Pharmacological analysis of epithelial chloride secretion mechanisms in adult murine airways

Blouquit, 2006, Ion and fluid transport properties of small airways in cystic fibrosis, Am. J. Respir. Crit. Care Med., 174, 299, 10.1164/rccm.200506-987OC Boedtkjer, 2015, New selective inhibitors of calcium-activated chloride channels-T16A(inh)-A01, CaCC(inh)-A01 and MONNA – what do they inhibit?, Br. J. Pharmacol., 172, 4158, 10.1111/bph.13201 Bradley, 2014, Pharmacological characterization of TMEM16A currents, Channels, 8, 308, 10.4161/chan.28065 Caputo, 2008, TMEM16A, a membrane protein associated with calcium-dependent chloride channel activity, Science, 322, 590, 10.1126/science.1163518 Colledge, 1996, Generation and characterization of a deltaF508 cystic fibrosis mousemodel, Nat. Genet., 10, 445, 10.1038/ng0895-445 De La Fuente, 2008, Small-molecule screen identifies inhibitors of a human intestinal calcium-activated chloride channel, Mol. Pharmacol., 73, 758, 10.1124/mol.107.043208 Flores, 2010, Strain-dependent differences in electrogenic secretion of electrolytes across mouse colon epithelium, Exp. Physiol., 95, 686, 10.1113/expphysiol.2009.051102 French, 1995, Isotype-specific activation of cystic fibrosis transmembrane conductance regulator-chloride channels by cGMP-dependent protein Kinase II, J. Biol. Chem., 270, 26626, 10.1074/jbc.270.44.26626 Grandoch, 2010, The role of Epac proteins, novel cAMP mediators, in the regulation of immune, lung and neuronal function, Br. J. Pharmacol., 159, 265, 10.1111/j.1476-5381.2009.00458.x Grubb, 1994, Anomalies in ion transport in CF mouse tracheal epithelium, Am. J. Physiol., 267, C293, 10.1152/ajpcell.1994.267.1.C293 Grubb, 1999, Pathophysiology of gene-targeted mouse models for cystic fibrosis, Physiol. Rev., 79, S193, 10.1152/physrev.1999.79.1.S193 He, 2011, Activation of the basolateral membrane Cl− conductance essential for electrogenic K+ secretion suppresses electrogenic Cl− secretion, Exp. Physiol., 96, 305, 10.1113/expphysiol.2010.055038 Hoque, 2010, Epac1 mediates protein kinase A-independent mechanism of forskolin-activated intestinal chloride secretion, J. Gen. Physiol., 135, 43, 10.1085/jgp.200910339 Ivonet, 2014, Hydrogen peroxide stimulation of CFTR reveals an EPAC-mediated, soluble adenylyl cyclase dependent cAMP amplification pathway common to GPCR signaling, Br. J. Pharmacol., 172, 173, 10.1111/bph.12934 Lee, 2010, cAMP-activated Ca2+ signaling is required for CFTR-mediated serous cell fluid secretion in porcine and human airways, J. Clin. Investig., 120, 3137, 10.1172/JCI42992 Liu, 2015, Characterization of the effects of Cl− channel modulators on TMEM16A and bestrophin-1 Ca2+ activated Cl− channels, Pflug. Arch., 467, 1417, 10.1007/s00424-014-1572-5 Matsui, 1998, Evidence for periciliary liquid layer depletion, not abnormal ion composition, in the pathogenesis of cystic fibrosis airways disease, Cell, 95, 1005, 10.1016/S0092-8674(00)81724-9 Namkung, 2011, TMEM16A inhibitors reveal TMEM16A as a minor component of calcium-activated chloride channel conductance in airway and intestinal epithelial cells, J. Biol. Chem., 286, 2365, 10.1074/jbc.M110.175109 Ousingsawat, 2009, Loss of TMEM16A causes a defect in epithelial Ca2+-dependent chloride transport, J. Biol. Chem., 284, 28698, 10.1074/jbc.M109.012120 Pedemonte, 2014, Structure and function of TMEM16 proteins (anoctamins), Physiol. Rev., 94, 419, 10.1152/physrev.00039.2011 Rock, 2008, The transmembrane protein TMEM16A is required for normal development of the murine trachea, Dev. Biol., 321, 141, 10.1016/j.ydbio.2008.06.009 Rock, 2009, Transmembrane protein 16A (TMEM16A) is a Ca2+-regulated Cl− secretory channel in mouse airways, J. Biol. Chem., 284, 14875, 10.1074/jbc.C109.000869 Rozmahel, 1996, Modulation of disease severity in cystic fibrosis transmembrane conductance regulator deficient mice by a secondary genetic factor, Nat. Genet, 12, 280, 10.1038/ng0396-280 Scholte, 2004, Animal models of cystic fibrosis, J. Cyst. Fibros., 3, S183, 10.1016/j.jcf.2004.05.039 Schroeder, 2008, Expression cloning of TMEM16A as a calcium-activated chloride channel subunit, Cell, 134, 1019, 10.1016/j.cell.2008.09.003 Scudieri, 2012, Association of TMEM16A chloride channel overexpression with airway goblet cell metaplasia, J. Physiol., 590, 6141, 10.1113/jphysiol.2012.240838 Sondo, 2011, Rescue of the mutant CFTR chloride channel by pharmacological correctors and low temperature analyzed by gene expression profiling, Am. J. Physiol. Cell Physiol., 301, C872, 10.1152/ajpcell.00507.2010 Sondo, 2014, The TMEM16A chloride channel as an alternative therapeutic target in cystic fibrosis, Int. J. Biochem Cell Biol., 52, 73, 10.1016/j.biocel.2014.03.022 Tarran, 2002, Regulation of murine airway surface liquid volume by CFTR and Ca2+ activated Cl− conductances, J. Gen. Physiol., 120, 407, 10.1085/jgp.20028599 Tarran, 2005, Normal and cystic fibrosis airway surface liquid homeostasis, J. Biol. Chem., 280, 35751, 10.1074/jbc.M505832200 Van Doorninck, 1995, A mouse model for the cystic fibrosis delta F508 mutation, EMBO J., 14, 4403, 10.1002/j.1460-2075.1995.tb00119.x Yang, 2008, TMEM16A confers receptor-activated calcium-dependent chloride conductance, Nature, 455, 1210, 10.1038/nature07313