NDLI: The switch of intestinal Slc26 exchangers from anion absorptive to HCOFormula secretory mode is dependent on CFTR anion channel function.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Singh, Anurag Kumar Riederer, Brigitte Chen, Mingmin Xiao, Fang Krabbenhöft, Anja Engelhardt, Regina Nylander, Olof Soleimani, Manoocher Seidler, Ursula
Description	Country affiliation: Germany Author Affiliation: Singh AK ( Dept. of Gastroenterology, Hepatology and Endocrinology, Hannover Medical School, Germany.)
Abstract	CFTR has been recognized to function as both an anion channel and a key regulator of Slc26 anion transporters in heterologous expression systems. Whether this regulatory relationship between CFTR and Slc26 transporters is seen in native intestine, and whether this effect is coupled to CFTR transport function or other features of this protein, has not been studied. The duodena of anesthetized CFTR-, NHE3-, Slc26a6-, and Scl26a3-deficient mice and wild-type (WT) littermates were perfused, and duodenal bicarbonate (HCO(3)(-)) secretion (DBS) and fluid absorptive or secretory rates were measured. The selective NHE3 inhibitor S1611 or genetic ablation of NHE3 significantly reduced fluid absorptive rates and increased DBS. Slc26a6 (PAT1) or Slc26a3 (DRA) ablation reduced the S1611-induced DBS increase and reduced fluid absorptive rates, suggesting that the effect of S1611 or NHE3 ablation on HCO(3)(-) secretion may be an unmasking of Slc26a6- and Slc26a3-mediated Cl(-)/HCO(3)(-) exchange activity. In the absence of CFTR expression or after application of the CFTR(inh)-172, fluid absorptive rates were similar to those of WT, but S1611 induced virtually no increase in DBS, demonstrating that CFTR transport activity, and not just its presence, is required for Slc26-mediated duodenal HCO(3)(-) secretion. A functionally active CFTR is an absolute requirement for Slc26-mediated duodenal HCO(3)(-) secretion, but not for Slc26-mediated fluid absorption, in which these transporters operate in conjunction with the Na(+)/H(+) exchanger NHE3. This suggests that Slc26a6 and Slc26a3 need proton recycling via NHE3 to operate in the Cl(-) absorptive mode and Cl(-) exit via CFTR to operate in the HCO(3)(-) secretory mode.
File Format	HTM / HTML
ISSN	03636143
e-ISSN	15221563
DOI	10.1152/ajpcell.00454.2009
Journal	American Journal of Physiology - Cell Physiology
Issue Number	5
Volume Number	298
Language	English
Publisher	American Physiological Society
Publisher Date	2010-05-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Discipline Cell Biology Antiporters Metabolism Cystic Fibrosis Transmembrane Conductance Regulator Physiology Animals Benzoates Pharmacology Bicarbonates Duodenum Gene Expression Regulation Drug Effects Intestinal Mucosa Mice Mice, Inbred Cftr Rna, Messenger Genetics Sodium-hydrogen Antiporter Thiazolidines Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't
Content Type	Text
Resource Type	Article
Subject	Cell Biology Physiology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

CFTR - a gatekeeper for duodenal HCO3- secretion.

The switch of intestinal Slc26 exchangers from anion absorptive to HCO3 − secretory mode is dependent on CFTR anion channel function

Differential activation of the HCO(3)(-) conductance through the cystic fibrosis transmembrane conductance regulator anion channel by genistein and forskolin in murine duodenum.

Assessment of cystic fibrosis transmembrane conductance regulator (CFTR) activity in CFTR-null mice after bone marrow transplantation.

Importance of SLC26 Transmembrane Anion Exchangers in Sperm Post-testicular Maturation and Fertilization Potential

Parathyroid hormone (PTH) rapidly enhances CFTR-mediated HCO3â» secretion in intestinal epithelium-like Caco-2 monolayer: a novel ion regulatory action of PTH.

Involvement of phosphatidylinositol 3-kinase in cAMP- and cGMP-induced duodenal epithelial CFTR activation in mice.

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice.

Revisiting CFTR inhibition: a comparative study of $CFTR_{inh}-172$ and GlyH-101 inhibitors

The switch of intestinal Slc26 exchangers from anion absorptive to HCOFormula secretory mode is dependent on CFTR anion channel function.

Similar Documents

CFTR - a gatekeeper for duodenal HCO3- secretion.

The switch of intestinal Slc26 exchangers from anion absorptive to HCO3 − secretory mode is dependent on CFTR anion channel function

Differential activation of the HCO(3)(-) conductance through the cystic fibrosis transmembrane conductance regulator anion channel by genistein and forskolin in murine duodenum.

Assessment of cystic fibrosis transmembrane conductance regulator (CFTR) activity in CFTR-null mice after bone marrow transplantation.

Importance of SLC26 Transmembrane Anion Exchangers in Sperm Post-testicular Maturation and Fertilization Potential

Parathyroid hormone (PTH) rapidly enhances CFTR-mediated HCO3â» secretion in intestinal epithelium-like Caco-2 monolayer: a novel ion regulatory action of PTH.

Involvement of phosphatidylinositol 3-kinase in cAMP- and cGMP-induced duodenal epithelial CFTR activation in mice.

Cystic fibrosis transmembrane conductance regulator dysfunction in VIP knockout mice.

Revisiting CFTR inhibition: a comparative study of $CFTR_{inh}-172$ and GlyH-101 inhibitors

The switch of intestinal Slc26 exchangers from anion absorptive to HCOFormula secretory mode is dependent on CFTR anion channel function.

Parathyroid hormone (PTH) rapidly enhances CFTR-mediated HCO3â» secretion in intestinal epithelium-like Caco-2 monolayer: a novel ion regulatory action of PTH.