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1 Department of Physiology, University of Oklahoma Health Science Center, Oklahoma City, OK, USA
2 Oklahoma Medical Research Foundation, University of Oklahoma Health Science Center, Oklahoma City, OK, USA
* To whom correspondence should be addressed. E-mail: hamid-akbarali{at}ouhsc.edu.
The ATP-sensitive K+ channel (KATP) is a complex composed of an inwardly-rectifying poreforming subunit (Kir 6.1 and Kir 6.2) and the sulphonylurea receptor (SUR1 and SUR2). In gastrointestinal smooth muscle, these channels are important in regulating cell excitability. We examined the molecular composition of the KATP channel in mouse colonic smooth muscle and determined its activity in the pathophysiological setting of experimental colitis. Following 7 days of dextran sulphate sodium (DSS) treatment in drinking water, colonic inflammation was scored by histology and physical signs. In whole-cell recordings, levcromakalim-induced currents were significantly larger in inflamed cells. In cell-attached patch recordings of single channel events, levcromakalim enhanced the bursting duration in inflamed cells. The single channel conducatance of ~42 pS was not altered with inflammation. mRNA for both Kir 6.1 and 6.2 were detected by RT-PCR. Kir 6.1 was localized to the plasma membrane while Kir 6.2 was mainly detected in the cytosol by immunohistochemistry. Quantitative PCR showed that Kir 6.1 gene expression was upregulated by almost 22 fold while SUR2B was downregulated by 3 fold following inflammation. Thus, decreased motility of the colon during inflammation may be associated with changes in the transcriptional regulation of Kir6.1 and SUR2B gene expression.
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