Abstract
KCNE1 (IsK, minK) co-assembles with KCNQI (KvLQT1) to form voltage-dependent K+ channels. Both KCNQ1 and KCNE1 are expressed in epithelial cells of gut and exocrine pancreas. We examined the role of KCNQ1/KCNE1 in Cl- secretion in small and large intestine and exocrine pancreas using the KCNE1 knockout mouse. Immunofluorescence revealed a similar basolateral localization of KCNQ1 in jejunum and colon of KCNE1 wild-type and knockout mice. Electrogenic Cl- secretion in the colon was not affected by gene disruption of KCNE1; in jejunum forskolin-induced short-circuit current was some 40% smaller but without being significantly different. Inhibition of KCNQ1 channels by 293B (IC50 1 μmol l-1) and by IKS224 (IC50 14 nmol l-1) strongly diminished intestinal Cl- secretion. In exocrine pancreas of wild-type mice, KCNQ1 was predominantly located at the basolateral membrane. In KCNE1 knockout mice, however, the basolateral staining was less pronounced and the distribution of secretory granules was irregular. A slowly activating and 293B-sensitive K+ current was activated via cholinergic stimulation in pancreatic acinar cells of wild-type mice. In KCNE1 knockout mice this K+ current was strongly reduced. In conclusion intestinal Cl- secretion is independent from KCNE1 but requires KCNQ1. In mouse pancreatic acini KCNQ1 probably co-assembled with KCNE1 leads to a voltage-dependent K+ current that might be of importance for electrolyte and enzyme secretion.
Original language | English (US) |
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Pages (from-to) | 822-828 |
Number of pages | 7 |
Journal | Pflugers Archiv European Journal of Physiology |
Volume | 443 |
Issue number | 5-6 |
DOIs | |
State | Published - 2002 |
Externally published | Yes |
Keywords
- Diarrhoea
- IsK
- KCNE3
- KvLQT1
- Mink
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Physiology (medical)