Hypotonic shock modulates Na(+) current via a Cl(-) and Ca(2+)/calmodulin dependent mechanism in alveolar epithelial cells
| Autor: | Emmanuelle Brochiero, Marie-Claude Tessier, Yves Berthiaume, Ryszard Grygorczyk, André Dagenais, Sabina Tatur |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2013 |
| Předmět: |
Male
Epithelial sodium channel medicine.medical_specialty Calmodulin lcsh:Medicine Biology Rats Sprague-Dawley 03 medical and health sciences Adenosine Triphosphate 0302 clinical medicine Chlorides Osmotic Pressure Internal medicine medicine Animals Transcellular lcsh:Science 030304 developmental biology 0303 health sciences Multidisciplinary Apyrase Sodium lcsh:R Epithelial Cells Potassium channel Rats Amiloride Pulmonary Alveoli Hypotonic Shock Endocrinology Calcium-Calmodulin-Dependent Protein Kinases biology.protein Biophysics Respiratory epithelium Calcium lcsh:Q 030217 neurology & neurosurgery Signal Transduction Research Article medicine.drug |
| Zdroj: | PLoS ONE, Vol 8, Iss 9, p e74565 (2013) PLoS ONE |
| ISSN: | 1932-6203 |
| Popis: | Alveolar epithelial cells are involved in Na(+) absorption via the epithelial Na(+) channel (ENaC), an important process for maintaining an appropriate volume of liquid lining the respiratory epithelium and for lung oedema clearance. Here, we investigated how a 20% hypotonic shock modulates the ionic current in these cells. Polarized alveolar epithelial cells isolated from rat lungs were cultured on permeant filters and their electrophysiological properties recorded. A 20% bilateral hypotonic shock induced an immediate, but transient 52% rise in total transepithelial current and a 67% increase in the amiloride-sensitive current mediated by ENaC. Amiloride pre-treatment decreased the current rise after hypotonic shock, showing that ENaC current is involved in this response. Since Cl(-) transport is modulated by hypotonic shock, its contribution to the basal and hypotonic-induced transepithelial current was also assessed. Apical NPPB, a broad Cl(-) channel inhibitor and basolateral DIOA a potassium chloride co-transporter (KCC) inhibitor reduced the total and ENaC currents, showing that transcellular Cl(-) transport plays a major role in that process. During hypotonic shock, a basolateral Cl(-) influx, partly inhibited by NPPB is essential for the hypotonic-induced current rise. Hypotonic shock promoted apical ATP secretion and increased intracellular Ca(2+). While apyrase, an ATP scavenger, did not inhibit the hypotonic shock current response, W7 a calmodulin antagonist completely prevented the hypotonic current rise. These results indicate that a basolateral Cl(-) influx as well as Ca(2+)/calmodulin, but not ATP, are involved in the acute transepithelial current rise elicited by hypotonic shock. |
| Databáze: | OpenAIRE |
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