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Article ; Online: Calmodulin Antagonist W-7 Enhances Intermediate Conductance Ca

Bowley, Kate A / Sandle, Geoffrey I

2021 Volume 254, Issue 4, Page(s) 423–428

Abstract: Intermediate conductance potassium ( ... ...

Abstract	Intermediate conductance potassium (IK
MeSH term(s)	Calmodulin/metabolism ; Calmodulin/pharmacology ; Colon/metabolism ; Humans ; Potassium Channel Blockers/pharmacology ; Potassium Channels/metabolism ; Sulfonamides
Chemical Substances	Calmodulin ; Potassium Channel Blockers ; Potassium Channels ; Sulfonamides ; W 7 (65595-90-6)
Language	English
Publishing date	2021-07-27
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3082-x
ISSN	1432-1424 ; 0022-2631
ISSN (online)	1432-1424
ISSN	0022-2631
DOI	10.1007/s00232-021-00193-y
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Article ; Online: Is intestinal transport dysfunctional in COVID-19-related diarrhea?

Sandle, Geoffrey I / Herod, Morgan R / Fontana, Juan / Lippiat, Jonathan D / Stockley, Peter G

American journal of physiology. Gastrointestinal and liver physiology

2023 Volume 324, Issue 5, Page(s) G415–G418

Abstract: Diarrhea, often severe, is a recognized and frequently early symptom during acute COVID-19 infection and may persist or develop for the first time in patients with long-COVID, with socioeconomic consequences. Diarrheal mechanisms in these cases are ... ...

Abstract	Diarrhea, often severe, is a recognized and frequently early symptom during acute COVID-19 infection and may persist or develop for the first time in patients with long-COVID, with socioeconomic consequences. Diarrheal mechanisms in these cases are poorly understood. There is evidence for disruption of intestinal epithelial barrier function and also for changes in the gut microbiome, which is critical for gut immunity and metabolism. Whether the SARS-CoV-2 virus has adverse effects on intestinal transport proteins is unclear. However, the ability of the virus to inhibit expression and activity of an aldosterone-regulated epithelial sodium (Na
MeSH term(s)	Humans ; COVID-19 ; SARS-CoV-2/metabolism ; Epithelial Sodium Channels/metabolism ; Post-Acute COVID-19 Syndrome ; Diarrhea
Chemical Substances	Epithelial Sodium Channels
Language	English
Publishing date	2023-03-28
Publishing country	United States
Document type	Editorial
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00021.2023
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Article ; Online: Colonic Potassium Absorption and Secretion in Health and Disease.

Rajendran, Vazhaikkurichi M / Sandle, Geoffrey I

Comprehensive Physiology

2018 Volume 8, Issue 4, Page(s) 1513–1536

Abstract: The colon has large capacities for ... ...

Abstract	The colon has large capacities for K
MeSH term(s)	Animals ; Colon/metabolism ; Humans ; Intestinal Absorption ; Potassium/metabolism ; Potassium Channels/metabolism
Chemical Substances	Potassium Channels ; Potassium (RWP5GA015D)
Language	English
Publishing date	2018-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ISSN	2040-4603
ISSN (online)	2040-4603
DOI	10.1002/cphy.c170030
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Article ; Online: Infective and inflammatory diarrhoea: mechanisms and opportunities for novel therapies.

Sandle, Geoffrey I

Current opinion in pharmacology

2011 Volume 11, Issue 6, Page(s) 634–639

Abstract: There have been significant advances in unravelling the cellular mechanisms of diarrhoea in common gut infections and colonic inflammation, as well as in the identification of targets for potential antidiarrhoeal drugs. Infective diarrhoea reflects ... ...

Abstract	There have been significant advances in unravelling the cellular mechanisms of diarrhoea in common gut infections and colonic inflammation, as well as in the identification of targets for potential antidiarrhoeal drugs. Infective diarrhoea reflects activation of electrogenic Cl⁻ secretion, inhibition of electroneutral NaCl absorption and in some cases, downregulation of tight junctional proteins and increased apoptosis. In colonic inflammation, diarrhoea mainly reflects impairment of colonic Na⁺ and Cl⁻ absorption by inflammatory cytokines, leading to decreased water absorption. Stimulation of endogenous opiate-dependent pathways, manipulation of epithelial ion (Na⁺, K⁺ and Cl⁻) channels and suppression of proinflammatory cytokine production by a variety of drugs and novel molecules, offer opportunities to move evaluation of these potential antisecretory and anti-inflammatory agents from the laboratory into clinical trials.
MeSH term(s)	Animals ; Anti-Inflammatory Agents/pharmacology ; Anti-Inflammatory Agents/therapeutic use ; Antidiarrheals/pharmacology ; Antidiarrheals/therapeutic use ; Cytokines/metabolism ; Diarrhea/etiology ; Diarrhea/prevention & control ; Dysentery/drug therapy ; Dysentery/metabolism ; Dysentery/physiopathology ; Humans ; Inflammatory Bowel Diseases/drug therapy ; Inflammatory Bowel Diseases/metabolism ; Inflammatory Bowel Diseases/physiopathology ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Ion Channels/agonists ; Ion Channels/antagonists & inhibitors ; Molecular Targeted Therapy ; Signal Transduction/drug effects
Chemical Substances	Anti-Inflammatory Agents ; Antidiarrheals ; Cytokines ; Ion Channels
Language	English
Publishing date	2011-12
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.09.005
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Article ; Online: Liddle-Mutation of the β-Subunit, but not the γ-Subunit, Attenuates Protein Kinase C-Mediated Inhibition of Human Epithelial Sodium Channels (hENaC).

Robins, Gerard G / Sandle, Geoffrey I

The Journal of membrane biology

2016 Volume 249, Issue 3, Page(s) 271–279

Abstract: Mammalian distal nephron and distal colon, prime sites for Na(+) homeostasis, contain amiloride-sensitive epithelial sodium channels (ENaC). Protein kinase C (PKC) inhibits ENaC by phosphorylating serine and threonine residues within COOH termini of the ... ...

Abstract	Mammalian distal nephron and distal colon, prime sites for Na(+) homeostasis, contain amiloride-sensitive epithelial sodium channels (ENaC). Protein kinase C (PKC) inhibits ENaC by phosphorylating serine and threonine residues within COOH termini of the β- and/or γ-subunits. Although some of these phosphorylation sites are close to the PY motifs, it is unclear whether they remain susceptible to PKC in Liddle-mutated ENaC β- and/or γ-subunits, where PY motifs are truncated, resulting in increased apical ENaC expression. We therefore studied the effects of PKC in wild-type and Liddle-mutated human epithelial Na(+) channels (hENaC) expressed in Xenopus oocytes, using the dual-electrode voltage clamp technique. PKC activation using 500 nmol/l phorbol 12-myristate 13-acetate (PMA) decreased amiloride-sensitive Na(+) currents by 80 % in oocytes expressing wild-type hENaC, an effect largely prevented by co-exposure to 50 µmol/l calphostin C (a specific inhibitor of PKC), whereas 500 nmol/l phorbol didecanoate (PDD), an inactive phorbol ester which does not stimulate PKC, had no effect. In oocytes expressing hENaC containing the Liddle-mutated β-subunit, PMA elicited a 54 % decrease in amiloride-sensitive Na(+) currents, significantly (P < 0.0025) less than that in oocytes expressing wild-type hENaC. By contrast, in oocytes expressing hENaC containing the Liddle-mutated γ-subunit, PMA elicited a 68 % decrease in amiloride-sensitive Na(+) current, similar (P = 0.10) to that in oocytes expressing wild-type hENaC. We conclude that hENaC incorporating the Liddle-mutated β-subunit lacks one or more PKC phosphorylation sites, thereby significantly reducing the inhibitory effect of PKC on Na(+) channel activity, whereas hENaC incorporating Liddle-mutated γ-subunits remains as susceptible to PKC as wild-type hENaC.
MeSH term(s)	Animals ; Epithelial Sodium Channels/metabolism ; Humans ; Kidney/metabolism ; Mutation ; Naphthalenes/pharmacology ; Oocytes/metabolism ; Patch-Clamp Techniques ; Phorbol Esters/pharmacology ; Protein Interaction Domains and Motifs/genetics ; Protein Kinase C/chemistry ; Protein Kinase C/genetics ; Protein Kinase C/metabolism ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Xenopus laevis
Chemical Substances	Epithelial Sodium Channels ; Naphthalenes ; Phorbol Esters ; Protein Subunits ; phorbol-12-myristate (20839-06-9) ; Protein Kinase C (EC 2.7.11.13) ; calphostin C (I271P23G24)
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3082-x
ISSN	1432-1424 ; 0022-2631
ISSN (online)	1432-1424
ISSN	0022-2631
DOI	10.1007/s00232-015-9866-x
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Article ; Online: Calcium rapidly down-regulates human renal epithelial sodium channels via a W-7-sensitive mechanism.

Robins, Gerard G / Sandle, Geoffrey I

The Journal of membrane biology

2014 Volume 247, Issue 8, Page(s) 729–737

Abstract: Increases in intracellular calcium (Ca(2+)) inhibit renal sodium (Na(+)) absorption in cortical collecting ducts, but the precise mechanism is unclear. We, therefore, studied the effects of raising intracellular Ca(2+) (using 10 µmol/L A23187, a Ca(2+) ... ...

Abstract	Increases in intracellular calcium (Ca(2+)) inhibit renal sodium (Na(+)) absorption in cortical collecting ducts, but the precise mechanism is unclear. We, therefore, studied the effects of raising intracellular Ca(2+) (using 10 µmol/L A23187, a Ca(2+) ionophore) on wild-type and Liddle-mutated human epithelial Na(+) channels (hENaC) expressed in Xenopus oocytes, using the dual-electrode voltage clamp technique. A23187 decreased amiloride-sensitive Na(+) current by 55% in oocytes expressing wild-type hENaC, an effect prevented by co-exposure to 50 μmol/L W-7 (to inhibit the Ca(2+)/calmodulin complex). By contrast, co-exposure to 50 μmol/L calphostin (to inhibit protein kinase C) or 5 μmol/L KN-62 (to inhibit Ca(2+)/calmodulin-dependent protein kinase II) had no effect on the decrease in amiloride-sensitive Na(+) current elicited by A23187 alone. Whereas A23187 reduced amiloride-sensitive Na(+) current in oocytes expressing wild-type hENaC, it had no similar effect in those expressing Liddle-mutated hENaCs, suggesting that the activity of individual Na(+) channels in situ was unchanged by the rise in intracellular Ca(2+). These data suggest that the A23187-induced rise in intracellular Ca(2+) inhibited wild-type hENaC through a W-7-sensitive mechanism, which likely reflected enhanced removal of Na(+) channels from the cell membrane by endocytosis. We, therefore, propose that Na(+) absorption in cortical collecting duct cells is inhibited by Ca(2+), possibly when complexed with calmodulin.
MeSH term(s)	Animals ; Calcium/pharmacology ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors ; Cell Membrane/drug effects ; Cell Membrane/metabolism ; Endocytosis/drug effects ; Endocytosis/physiology ; Enzyme Inhibitors/pharmacology ; Epithelial Sodium Channels/chemistry ; Epithelial Sodium Channels/metabolism ; Female ; Humans ; Kidney/cytology ; Kidney/drug effects ; Kidney/metabolism ; Oocytes/cytology ; Oocytes/drug effects ; Oocytes/metabolism ; Patch-Clamp Techniques ; Sodium/metabolism ; Sulfonamides/pharmacology ; Xenopus laevis
Chemical Substances	Enzyme Inhibitors ; Epithelial Sodium Channels ; Sulfonamides ; W 7 (65595-90-6) ; Sodium (9NEZ333N27) ; Calcium-Calmodulin-Dependent Protein Kinases (EC 2.7.11.17) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2014-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3082-x
ISSN	1432-1424 ; 0022-2631
ISSN (online)	1432-1424
ISSN	0022-2631
DOI	10.1007/s00232-014-9698-0
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Article: Infective and inflammatory diarrhoea: mechanisms and opportunities for novel therapies

Sandle, Geoffrey I

Current opinion in pharmacology. 2011 Dec., v. 11, no. 6

2011

Abstract	There have been significant advances in unravelling the cellular mechanisms of diarrhoea in common gut infections and colonic inflammation, as well as in the identification of targets for potential antidiarrhoeal drugs. Infective diarrhoea reflects activation of electrogenic Cl⁻ secretion, inhibition of electroneutral NaCl absorption and in some cases, downregulation of tight junctional proteins and increased apoptosis. In colonic inflammation, diarrhoea mainly reflects impairment of colonic Na⁺ and Cl⁻ absorption by inflammatory cytokines, leading to decreased water absorption. Stimulation of endogenous opiate-dependent pathways, manipulation of epithelial ion (Na⁺, K⁺ and Cl⁻) channels and suppression of proinflammatory cytokine production by a variety of drugs and novel molecules, offer opportunities to move evaluation of these potential antisecretory and anti-inflammatory agents from the laboratory into clinical trials.
Keywords	absorption ; anti-inflammatory agents ; apoptosis ; clinical trials ; cytokines ; diarrhea ; digestive system ; inflammation ; potassium ; proteins ; secretion ; sodium ; sodium chloride
Language	English
Dates of publication	2011-12
Size	p. 634-639.
Publishing place	Elsevier Ltd
Document type	Article
ZDB-ID	2037057-X
ISSN	1471-4973 ; 1471-4892
ISSN (online)	1471-4973
ISSN	1471-4892
DOI	10.1016/j.coph.2011.09.005
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Cyclic AMP-induced K+ secretion occurs independently of Cl- secretion in rat distal colon.

Sandle, Geoffrey I / Rajendran, Vazhaikkurichi M

American journal of physiology. Cell physiology

2012 Volume 303, Issue 3, Page(s) C328–33

Abstract: cAMP induces both active Cl(-) and active K(+) secretion in mammalian colon. It is generally assumed that a mechanism for K(+) exit is essential to maintain cells in the hyperpolarized state, thus favoring a sustained Cl(-) secretion. Both Kcnn4c and ... ...

Abstract	cAMP induces both active Cl(-) and active K(+) secretion in mammalian colon. It is generally assumed that a mechanism for K(+) exit is essential to maintain cells in the hyperpolarized state, thus favoring a sustained Cl(-) secretion. Both Kcnn4c and Kcnma1 channels are located in colon, and this study addressed the questions of whether Kcnn4c and/or Kcnma1 channels mediate cAMP-induced K(+) secretion and whether cAMP-induced K(+) secretion provides the driving force for Cl(-) secretion. Forskolin (FSK)-enhanced short-circuit current (indicator of net electrogenic ion transport) and K(+) fluxes were measured simultaneously in colonic mucosa under voltage-clamp conditions. Mucosal Na(+) orthovanadate (P-type ATPase inhibitor) inhibited active K(+) absorption normally present in rat distal colon. In the presence of mucosal Na(+) orthovanadate, serosal FSK induced both K(+) and Cl(-) secretion. FSK-induced K(+) secretion was 1) not inhibited by either mucosal or serosal 1-[(2-chlorophenyl) diphenylmethyl]-1H-pyrazole (TRAM-34; a Kcnn4 channel blocker), 2) inhibited (92%) by mucosal iberiotoxin (Kcnma1 channel blocker), and 3) not affected by mucosal cystic fibrosis transmembrane conductance regulator inhibitor (CFTR(inh)-172). By contrast, FSK-induced Cl(-) secretion was 1) completely inhibited by serosal TRAM-34, 2) not inhibited by either mucosal or serosal iberiotoxin, and 3) completely inhibited by mucosal CFTR(inh)-172. These results indicate that cAMP-induced colonic K(+) secretion is mediated via Kcnma1 channels located in the apical membrane and most likely contributes to stool K(+) losses in secretory diarrhea. On the other hand, cAMP-induced colonic Cl(-) secretion requires the activity of Kcnn4b channels located in the basolateral membrane and is not dependent on the concurrent activation of apical Kcnma1 channels.
MeSH term(s)	Animals ; Chlorides/metabolism ; Colforsin/pharmacology ; Colon/drug effects ; Colon/metabolism ; Cyclic AMP/metabolism ; Cystic Fibrosis Transmembrane Conductance Regulator/antagonists & inhibitors ; Cystic Fibrosis Transmembrane Conductance Regulator/metabolism ; Intermediate-Conductance Calcium-Activated Potassium Channels/antagonists & inhibitors ; Intermediate-Conductance Calcium-Activated Potassium Channels/metabolism ; Intestinal Mucosa/drug effects ; Intestinal Mucosa/metabolism ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/antagonists & inhibitors ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism ; Male ; Peptides/pharmacology ; Potassium/metabolism ; Pyrazoles/pharmacology ; Rats ; Rats, Sprague-Dawley ; Vanadates/pharmacology
Chemical Substances	Chlorides ; Intermediate-Conductance Calcium-Activated Potassium Channels ; Kcnma1 protein, rat ; Kcnn4 protein, rat ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Peptides ; Pyrazoles ; TRAM 34 ; Cystic Fibrosis Transmembrane Conductance Regulator (126880-72-6) ; Colforsin (1F7A44V6OU) ; Vanadates (3WHH0066W5) ; iberiotoxin (773HER9B6T) ; Cyclic AMP (E0399OZS9N) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2012-05-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	392098-7
ISSN	1522-1563 ; 0363-6143
ISSN (online)	1522-1563
ISSN	0363-6143
DOI	10.1152/ajpcell.00099.2012
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Article: Pathogenesis of diarrhea in ulcerative colitis: new views on an old problem.

Sandle, Geoffrey I

Journal of clinical gastroenterology

2005 Volume 39, Issue 4 Suppl 2, Page(s) S49–52

Abstract: Background: Whereas water movement into the intestinal lumen occurs secondary to Cl secretion in secretory diarrheal diseases, defects in key transport processes lead to profound decreases in colonic Na, Cl, and water absorption in ulcerative colitis.!## ...

Abstract	Background: Whereas water movement into the intestinal lumen occurs secondary to Cl secretion in secretory diarrheal diseases, defects in key transport processes lead to profound decreases in colonic Na, Cl, and water absorption in ulcerative colitis. Studies and results: Recent studies indicate reduced expression/activity of apical Na channels and basolateral Na, K-ATPase, leading to loss of electrogenic Na absorption in the distal colon and rectum. There is also likely to be a decrease in electroneutral NaCl cotransport, which is present throughout the colon. Preliminary work on basolateral K channel abundance and activity in colonic epithelial cells suggests that whole-cell K conductance is decreased in ulcerative colitis, leading to epithelial cell depolarization, and further limitation of Na absorption. In addition, there is a marked reduction in colonic epithelial resistance, which reflects a decrease in the integrity of intercellular tight junctions and the presence of apoptotic foci. Conclusions: Impaired Na and Cl transport, combined with enhanced epithelial "leakiness," results in a profound decrease in the capacity of the inflamed colon to absorb salt and water. Transport abnormalities in ulcerative colitis may at least partly reflect the effects of proinflammatory cytokines, raising the possibility of novel approaches to the restoration of colonic absorptive capacity in this disease.
MeSH term(s)	Biological Transport ; Chlorides/metabolism ; Colitis, Ulcerative/complications ; Colitis, Ulcerative/physiopathology ; Diarrhea/etiology ; Diarrhea/physiopathology ; Humans ; Intestinal Absorption/physiology ; Potassium/metabolism ; Sodium/metabolism ; Water-Electrolyte Balance
Chemical Substances	Chlorides ; Sodium (9NEZ333N27) ; Potassium (RWP5GA015D)
Language	English
Publishing date	2005-01-28
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	448460-5
ISSN	1539-2031 ; 0192-0790
ISSN (online)	1539-2031
ISSN	0192-0790
DOI	10.1097/01.mcg.0000155520.04253.37
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Article ; Online: Parallel intermediate conductance K

Rehman, Shabina / Narayanan, Karthikeyan / Nickerson, Andrew J / Coon, Steven D / Hoque, Kazi Mirajul / Sandle, Geoffrey I / Rajendran, Vazhaikkurichi M

American journal of physiology. Gastrointestinal and liver physiology

2020 Volume 319, Issue 2, Page(s) G142–G150

Abstract: Transepithelial ... ...

Abstract	Transepithelial K
MeSH term(s)	Animals ; Chloride Channels/genetics ; Chloride Channels/metabolism ; Chlorides/metabolism ; Colon/physiology ; Female ; Intestinal Mucosa/metabolism ; Ion Transport ; Male ; Patch-Clamp Techniques ; Potassium/metabolism ; Potassium Channels/genetics ; Potassium Channels/metabolism ; Protein Transport ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Chloride Channels ; Chlorides ; Potassium Channels ; Potassium (RWP5GA015D)
Language	English
Publishing date	2020-06-22
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	603840-2
ISSN	1522-1547 ; 0193-1857
ISSN (online)	1522-1547
ISSN	0193-1857
DOI	10.1152/ajpgi.00011.2020
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