Literature DB >> 12475760

Cytoskeletal modulation of sodium current in human jejunal circular smooth muscle cells.

Peter R Strege1, Adrian N Holm, Adam Rich, Steven M Miller, Yijun Ou, Michael G Sarr, Gianrico Farrugia.   

Abstract

A Na(+) current is present in human jejunal circular smooth muscle cells. The aim of the present study was to determine the role of the cytoskeleton in the regulation of the Na(+) current. Whole cell currents were recorded by using standard patch-clamp techniques with Cs(+) in the pipette to block K(+) currents. Cytochalasin D and gelsolin were used to disrupt the actin cytoskeleton and phalloidin to stabilize it. Colchicine was used to disassemble the microtubule cytoskeleton (and intermediate filaments) and paclitaxel to stabilize it. Acrylamide was used to disrupt the intermediate filament cytoskeleton. Perfusion of the recording chamber at 10 ml/min increased peak Na(+) current recorded from jejunal smooth muscle cells by 27 +/- 3%. Cytochalasin D and gelsolin abolished the perfusion-induced increase in Na(+) current, whereas incubation with phalloidin, colchicine, paclitaxel, or acrylamide had no effect. In conclusion, the Na(+) current expressed in human jejunal circular smooth muscle cells appears to be regulated by the cytoskeleton. An intact actin cytoskeleton is required for perfusion-induced activation of the Na(+) current.

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Year:  2003        PMID: 12475760     DOI: 10.1152/ajpcell.00532.2001

Source DB:  PubMed          Journal:  Am J Physiol Cell Physiol        ISSN: 0363-6143            Impact factor:   4.249


  33 in total

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Review 5.  Gastrointestinal motility and its enteric actors in mechanosensitivity: past and present.

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Review 7.  Mechanosensitive Piezo Channels in the Gastrointestinal Tract.

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8.  Lysophosphatidyl choline modulates mechanosensitive L-type Ca2+ current in circular smooth muscle cells from human jejunum.

Authors:  Robert E Kraichely; Peter R Strege; Michael G Sarr; Michael L Kendrick; Gianrico Farrugia
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9.  Sodium channel mutation in irritable bowel syndrome: evidence for an ion channelopathy.

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10.  Lack of serotonin 5-HT2B receptor alters proliferation and network volume of interstitial cells of Cajal in vivo.

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