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©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastrointest Pathophysiol. Feb 15, 2016; 7(1): 138-149
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.138
Published online Feb 15, 2016. doi: 10.4291/wjgp.v7.i1.138
Differential expression of pancreatic protein and chemosensing receptor mRNAs in NKCC1-null intestine
Emily M Bradford, Department of Internal Medicine, Division of Gastroenterology, University of Kentucky, Lexington, KY 40536-0298, United States
Kanimozhi Vairamani, Gary E Shull, Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, Cincinnati, OH 45267-0524, United States
Author contributions: Bradford EM and Shull GE conceived the study, analyzed the data, and wrote the manuscript; Vairamani K analyzed and compiled microarray data; Bradford EM performed all of the experiments.
Supported by National Institutes of Health to Gary E Shull, No. DK050594.
Institutional review board statement: Because human subjects or tissues were not used in this study, approval from the institutional review board was not required. Ethical issues relating to the animal protocol were reviewed and approved by the Institutional Animal Care and Use Committee of the University of Cincinnati.
Institutional animal care and use committee statement: All procedures involving animals were reviewed and approved by the Institutional Animal Care and Use Committee (IACUC) of the University of Cincinnati (protocol number: 06-06-22-02).
Conflict-of-interest statement: The authors have no conflict of interest related to this manuscript.
Data sharing statement: The microarray data have been deposited in the National Center for Biotechnology Gene Expression Omnibus and can be freely accessed as described in Methods. The Slc12a2 (NKCC1) knockout mouse model has been deposited in a publically available repository and can be accessed as described in Methods.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Gary E Shull, PhD, Professor, Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati College of Medicine, 231 Albert Sabin Way, Cincinnati, OH 45267-0524, United States. shullge@ucmail.uc.edu
Telephone: +1-513-5580056 Fax: +1-513-5591885
Received: June 29, 2015
Peer-review started: July 2, 2015
First decision: September 22, 2015
Revised: October 10, 2015
Accepted: December 17, 2015
Article in press: December 18, 2015
Published online: February 15, 2016
Peer-review started: July 2, 2015
First decision: September 22, 2015
Revised: October 10, 2015
Accepted: December 17, 2015
Article in press: December 18, 2015
Published online: February 15, 2016
Core Tip
Core tip: The NKCC1 Na+-K+-2Cl- cotransporter is a major mechanism of Cl- uptake in support of secretion. To investigate its intestinal functions we analyzed mRNA expression changes in NKCC1-null intestines. Differentially expressed genes included digestive enzymes and a large number of olfactory and other G-protein coupled receptors that function in chemical sensing. This suggests that loss of NKCC1 affects not only secretion, but also digestion and chemosensing of components of the intestinal contents. The results likely have relevance to recent evidence showing that mutations in the human NKCC1 gene cause unexplained food intolerance and failure of intestinal function requiring parenteral nutrition.