Intestinal Secretion and Barrier Function; Implication with Muscarinic Cholinoceptor
American Journal of Life Sciences
Volume 3, Issue 4, August 2015, Pages: 311-315
Received: Jun. 15, 2015;
Accepted: Jul. 11, 2015;
Published: Jul. 18, 2015
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Md. Rafiqul Islam Khan, Department of Biochemistry, Asahikawa Medical University, Hokkaido, Japan; Department of Pharmacy, University of Rajshahi, Rajshahi, Bangladesh
Takashi Yazawa, Department of Biochemistry, Asahikawa Medical University, Hokkaido, Japan
Junsuke Uwada, Department of Biochemistry, Asahikawa Medical University, Hokkaido, Japan
Abu Syed Md. Anisuzzaman, Department of Pharmacy, University of Rajshahi, Rajshahi, Bangladesh; Department of Hematology & Medical Oncology, Winship Cancer Institute, Emory University, Atlanta, USA
Takanobu Taniguchi, Department of Biochemistry, Asahikawa Medical University, Hokkaido, Japan
Two most important physiological functions of intestinal epithelial cells (IECs) are intestinal secretion and barrier function in order to protect the host from invasive microorganisms. Acetylcholine (ACh) is regarded as a central molecule for the regulation of these gut functions. Although, ACh is considered as a classical neurotransmitter, numerous studies report the synthesis and release of ACh from non-neuronal epithelial cells and are believed to regulate gut functions via cholinergic activation. Recently, it is established that IECs express M1 and M3 muscarinic acetylcholine receptors (mAChRs). Although, the role of M3 mAChR-mediated intestinal secretion in Ussing Chamber has been highly established, little is known about M1 mAChR-mediated intestinal secretion and barrier function. Here, we review the current knowledge about the functions of M1 and M3 mAChRs and their downstream signaling in the regulation of intestinal secretion and barrier function. We also discuss the role of mAChRs in IECs under inflammatory conditions.
Md. Rafiqul Islam Khan,
Abu Syed Md. Anisuzzaman,
Intestinal Secretion and Barrier Function; Implication with Muscarinic Cholinoceptor, American Journal of Life Sciences.
Vol. 3, No. 4,
2015, pp. 311-315.
Barrett KE and Keely SJ. Integrative physiology and pathophysiology of intestinal electrolyte transport. In: Physiology of the Gastrointestinal Tract, edited by Johnson LR, Barrett KE, Ghishan FK, Merchant JL, Said HM, Wood JD. San Diego, CA: Academic: 2006, 1931-1951.
Eckmann L, Stenson WF, Savidge TC, et al. Role of Intestinal Epithelial Cells in the Host Secretory Response to Infection by Invasive Bacteria. J. Clin. Invest. 1997, 100:296–309.
Binder HJ. Mechanisms of Diarrhea in Inflammatory Bowel Diseases. Ann N Y Acad Sci. 2009, 1165:285-293.
Barker JM and Liu E. Celiac Disease: Pathophysiology, Clinical Manifestations and Associated Autoimmune Conditions. Adv. Pediatr. 2008, 55:349–365.
Mandel LJ, Bacallao R and Zampighi G. Uncoupling of the molecular “fence” and paracellular “gate” functions in epithelial tight junctions. Nature, 1993, 361:552-555.
Podolsky DK. Mucosal immunity and inflammation. V. Innate mechanism of mucosal defense and repair: the best offence is a good defense,. Am. J. Physiol. Gastrointest. Liver Physiol. 1999, 277:495-499.
Hirota CL and Mckay DM. Cholinergic regulation of epithelial ion transport in the mammalian intestine. Br. J. Pharm. 2006, 149:463-479.
Khan MRI, Yazawa T, Anisuzzaman ASM, et al. Activation of focal adhesion kinase via M1 muscarinic acetylcholine receptor is required in restitution of intestinal barrier function after epithelial injury. Biochimica et Biophysica Acta. 2014, 1842:635–645.
Khan MRI, Anisuzzaman ASM, Semba S, et al. M1 is a major subtype of muscarinic acetylcholine receptors on mouse colonic epithelial cells. J Gastroenterol. 2013, 48:885-896.
Ishii M and Kurachi Y. Muscarinic acetylcholine receptors,. Curr. Pharm. Des. 2006, 12:3573-3581.
Caulfield MP and Birdsall NJ. International union of pharmacology. XVII. Classification of muscarinic acetylcholine receptors. Pharmacol. Rev. 1998, 50:279-290.
Burford NT and Nahorski SR. Muscarinic M1 receptor-stimulated adenylate cyclase activity in Chinese hamster ovary cells is mediated by Gs alpha and is not a consequence of phosphoinositidase C activation. Biochem. J. 1996, 315:883-888.
Qin K, Dong C, Wu G, et al. Inactive-state preassembly of Gq-coupled receptors and Gq heterotrimers. Nat Chem Biol. 2011, 7:740–747.
Barrett KE. New ways of thinking about (and teaching about) intestinal epithelial function. Adv Physiol Educ. 2008, 32:25–34.
Donnellan F, Keating N, Geoghegan P, et al. JNK mitogen-activated protein kinase limits calcium-dependent chloride secretion across colonic epithelial cells. Am J Physiol Gastrointest Liver Physiol. 2010, 298:37-44.
Hebb CO. Acetylcholine metabolism of nervous tissue. Pharmacol Rev. 1954, 6: 39–43.
Hebb CO and Whittaker VP. Intracellular distributions of acetylcholine and choline acetylase. . J Physiol. 1958, 142:187–196.
Eiden LE. The cholinergic gene locus. . J Neurochem. 1998, 70:2227–2240.
Vulcano M, Lombardi MG and Sales ME. Nonneuronal Cholinergic System in Breast Tumors and Dendritic Cells: Does It Improve or Worsen the Response to Tumor? Hindawi Publishing Corporation; ISRN Cell Biology, 2013:1-12.
Kummer W, Lips KS and Pfeil U. The epithelial cholinergic system of the airways. Histochem Cell Biol. 2008, 130:219–234.
Barrett KE and Keely SJ. Chloride secretion by the intestinal epithelium: molecular basis and regulatory aspects. . Annu Rev Physiol. 2000, 62: 535–572.
Kunzelmann K and Mall M. Electrolyte transport in the mammalian colon: mechanisms and implications for disease. Physiol Rev. 2002, 82 245–289.
Hirota CL and McKay DM. Loss of Ca2+ -mediated ion transport during colitis correlates with reduced ion transport responses to a Ca2+ -activated K+ channel opener. Br. J. Pharm. 2009, 156:1085-1097.
Ussing HH and Zerahn K. Active transport of sodium as the source of electric current in the short-circuited isolated frog skin. Acta Physiol. Scand. 1951, 23:110-127.
Tidball CS. Active chloride transport during intestinal secretion. Am J Physiol. 1961, 200:309-312.
Kachintorn U, Vajanaphanich M, Barrett KE, et al. Elevation of inositol tetrakisphosphate parallels inhibition of Ca2+ -dependent Cl– secretion in T84 cells Am. J. Physiol. 1993, 264:671-676.
Barrett KE. Bowditch lecture. Integrated regulation of intestinal epithelial transport: intercellular and intracellular pathways. Am. J. Physiol. 1997, 272:1069-1076.
Khan MRI, Islam MT, Yazawa T, et al. Muscarinic cholinoceptor-mediated activation of JNK negatively regulates intestinal secretion in mice. J. Pharmacol. Sci. 2015, 127:150-153.
Maloy KJ and Powrie F. Intestinal homeostasis and its breakdown in inflammatory bowel disease. Nature, 2011, 474:298-306.
Coskun M. Intestinal Epithelium in Inflammatory Bowel Disease. Front. Med. 2014, 1:24.
Shi XZ, Winston JH and Sarna SK. Differential immune and genetic responses in rat models of Crohn’s colitis and ulcerative colitis. Am. J. Physiol. Gastrointest. Liver Physiol. 2011, 300:41-51.
Ma Y, Semba S, Maemoto A, et al. Oxazolone-induced over-expression of focal adhesion kinase in colonic epithelial cells of colitis mouse model,. FEBS lett. 2010, 584:3949-3954.
Peterson LW and Artis D. Intestinal epithelial cells: regulators of barrier function and immune homeostasis. NATURE REVIEWS | IMMUNOLOGY, 2014, 14:141-153.
Mankertz J and Schulzke JD. Altered permeability in inflammatory bowel disease: pathophysiology and clinical implications. Curr. Opin. Gastroenterol. 2007, 23: 379–383.
Siu ER, Wong EW, Mruk DD, et al. An occludin-focal adhesion kinase protein complex at the blodd-testis barrier: a study using the cadmium model. Endocrinology, 2009, 150:3336-3344.
Ma Y, Semba S, Khan MRI, et al. Focal adhesion kinase regulates intestinal epithelial barrier function via redistribution of tight junction. Biochim. Biophys. Acta, 2013, 1832:151–159.
Calandrella SO, Barrett KE and Keely SJ. Transactivation of the epidermal growth factor receptor mediates muscarinic stimulation of focal adhesion kinase in intestinal epithelial cells. J. Cell. Physiol. 2005, 203:103–110.
Lesko S, Wessler I, Gäbel G, et al. Cholinergic modulation of epithelial itegrity in the proximal colon of pigs. Cells Tissues Organs. 2012.
Podolsky DK. The current future understanding of inflammatory bowel disease. Best Pract. Res. Clin. Gastroenterol. 2002, 16:933-943.
Neuman MG. Signaling for Inflammation and Repair in Inflammatory Bowel Disease. Romanian J. Gastroenterol. 2004, 13:309-314.
Madara JL and Stafford J. Interferon-γ directly affects barrier function. J. Clin. Invest. 1989, 83:724-727.
Watson CJ, Hoare CJ, Garrod DR, et al. Interferon-γ selectively increases epithelial permeability to large molecules by activating different populations of paracellular pores. J. Cell Sci. 2005, 118:5221-5230.
Boivin AM, Roy PK, Bradley A, et al. Mechanism of interferon-γ–induced increase in T84 intestinal epithelial tight junction. J. Inter. Cyt. Res. 2009, 29:45-54.
McKay DM, Watson JL, Wang A, et al. Phosphatidylinositol 3’-kinase is a critical mediator of interferon-γ-induced increases in enteric epithelial permeability. J. Pharmacol. Exp. Ther. 2007, 320:1013–1022.
Scharl M, Paul G, Barrett KE, et al. AMP-activated protein kinase mediates the interferon-γ-induced decrease in intestinal epithelial barrier function,. J. Biol. Chem. 2009, 284:27952–27963.