ArticleBiochemical and biophysical research communications2016
Upregulation of basolateral small conductance potassium channels (KCNQ1/KCNE3) in ulcerative colitis.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- The SIMDA framework maps PIP2-binding sites regulating the KCNQ1 channel.Nature communications · 2026Article
- KCNE gene family: From basic functions to diseases.Genes & diseases · 2026Review
- Mechanisms of KCNQ1 gating modulation by KCNE1/3 for cell-specific function.Cell research · 2025Article
- Transforming Cancer Diagnostics: The Emergence of Liquid Biopsy and Epigenetic Markers.MedComm · 2025Review
- Ion transport and epithelial barrier dysfunction in experimental models of ulcerative colitis.American journal of physiology. Gastrointestinal and liver physiology · 2025Review
- Causal linkage between type 2 diabetes mellitus and inflammatory bowel disease: an integrated Mendelian randomization study and bioinformatics analysis.Frontiers in endocrinology · 2024Article
- Article
- Kv7 Channels in Lung Diseases.Frontiers in physiology · 2020Review
- Colonic Potassium Absorption and Secretion in Health and Disease.Comprehensive Physiology · 2018Review
- KThe Journal of physiology · 2018Article
- Structural basis for KCNE3 modulation of potassium recycling in epithelia.Science advances · 2016Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBasolateral K(+) channels hyperpolarize colonocytes to ensure Na(+) (and thus water) absorption. Small conductance basolateral (KCNQ1/KCNE3) K(+) channels have never been evaluated in human colon. We therefore evaluated KCNQ1/KCNE3 channels in distal colonic crypts obtained from normal and active ulcerative colitis (UC) patients.
methodsKCNQ1 and KCNE3 mRNA levels were determined by qPCR, and KCNQ1/KCNE3 channel activity in normal and UC crypts, and the effects of forskolin (activator of adenylate cyclase) and UC-related proinflammatory cytokines on normal crypts, studied by patch clamp recording.
resultsWhereas KCNQ1 and KCNE3 mRNA expression was similar in normal and UC crypts, single 6.8 pS channels were seen in 36% of basolateral patches in normal crypts, and to an even greater extent (74% of patches, P < 0.001) in UC crypts, with two or more channels per patch. Channel activity was 10-fold higher (P < 0.001) in UC crypts, with a greater contribution to basolateral conductance (5.85 ± 0.62 mS cm(-2)) than in controls (0.28 ± 0.04 mS cm(-2), P < 0.001). In control crypts, forskolin and thromboxane A2 stimulated channel activity 30-fold and 10-fold respectively, while PGE2, IL-1β, and LTD4 had no effect.
conclusionsKCNQ1/KCNE3 channels make only a small contribution to basolateral conductance in normal colonic crypts, with increased channel activity in UC appearing insufficient to prevent colonic cell depolarization in this disease. This supports the proposal that defective Na(+) absorption rather than enhanced Cl(-) secretion, is the dominant pathophysiological mechanism of diarrhea in UC.
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