Hypotonic Regulation of Mouse Epithelial Sodium Channel in Xenopus laevis Oocytes
The regulation of the epithelial Na + channel (ENaC) during cell swelling is relevant in cellular processes in which cell volume changes occur, i.e., migration, proliferation and cell absorption. Its sensitivity to hypotonically induced swelling was investigated in the Xenopus oocyte expression syst...
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| Veröffentlicht in: | The Journal of membrane biology 2013-12, Vol.246 (12), p.949-958 |
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| creator | Galizia, Luciano Marino, Gabriela I. Ojea, Alejandro Kotsias, Basilio A. |
| description | The regulation of the epithelial Na
+
channel (ENaC) during cell swelling is relevant in cellular processes in which cell volume changes occur, i.e., migration, proliferation and cell absorption. Its sensitivity to hypotonically induced swelling was investigated in the
Xenopus
oocyte expression system with the injection of the three subunits of mouse ENaC. We used voltage-clamp techniques to study the amiloride-sensitive Na
+
currents (
I
Na
(amil)
) and video microscopic methodologies to assess oocyte volume changes. Under conditions of mild swelling (25 % reduced hypotonicity) inward current amplitude decreased rapidly over 1.5 min. In contrast, there was no change in current amplitude of H
2
O-injected oocytes to the osmotic insult.
I
Na
(amil)
kinetics analysis revealed a decrease in the slower inactivation time constant during the hypotonic stimuli. Currents from ENaC-injected oocytes were not sensitive to external Cl
−
reduction. Neither short- nor long-term cytochalasin D treatment affected the observed response. Oocytes expressing a DEG mutant β-ENaC subunit (β-S518K) with an open probability of 1 had reduced
I
Na
(amil)
hypotonic response compared to oocytes injected with wild-type ENaC subunits. Finally, during the hypotonic response ENaC-injected oocytes did not show a cell volume difference compared with water-injected oocytes. On this basis we suggest that hypotonicity-dependent ENaC inhibition is principally mediated through an effect on open probability of channels in the membrane. |
| doi_str_mv | 10.1007/s00232-013-9598-8 |
| format | Article |
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+
channel (ENaC) during cell swelling is relevant in cellular processes in which cell volume changes occur, i.e., migration, proliferation and cell absorption. Its sensitivity to hypotonically induced swelling was investigated in the
Xenopus
oocyte expression system with the injection of the three subunits of mouse ENaC. We used voltage-clamp techniques to study the amiloride-sensitive Na
+
currents (
I
Na
(amil)
) and video microscopic methodologies to assess oocyte volume changes. Under conditions of mild swelling (25 % reduced hypotonicity) inward current amplitude decreased rapidly over 1.5 min. In contrast, there was no change in current amplitude of H
2
O-injected oocytes to the osmotic insult.
I
Na
(amil)
kinetics analysis revealed a decrease in the slower inactivation time constant during the hypotonic stimuli. Currents from ENaC-injected oocytes were not sensitive to external Cl
−
reduction. Neither short- nor long-term cytochalasin D treatment affected the observed response. Oocytes expressing a DEG mutant β-ENaC subunit (β-S518K) with an open probability of 1 had reduced
I
Na
(amil)
hypotonic response compared to oocytes injected with wild-type ENaC subunits. Finally, during the hypotonic response ENaC-injected oocytes did not show a cell volume difference compared with water-injected oocytes. On this basis we suggest that hypotonicity-dependent ENaC inhibition is principally mediated through an effect on open probability of channels in the membrane.</description><identifier>ISSN: 0022-2631</identifier><identifier>EISSN: 1432-1424</identifier><identifier>DOI: 10.1007/s00232-013-9598-8</identifier><identifier>PMID: 24121666</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Actins - metabolism ; Animals ; Biochemistry ; Biological Transport ; Biomedical and Life Sciences ; Cellular biology ; Epithelial Sodium Channels - genetics ; Epithelial Sodium Channels - metabolism ; Female ; Gene Expression ; Human Physiology ; Kinetics ; Life Sciences ; Membrane Potentials ; Membranes ; Mice ; Oocytes - metabolism ; Osmotic Pressure ; Rodents ; Sodium - metabolism ; Xenopus laevis</subject><ispartof>The Journal of membrane biology, 2013-12, Vol.246 (12), p.949-958</ispartof><rights>Springer Science+Business Media New York 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-688babe6ba905fc038e57834bd7415be167d962fbf7006ebfc55b9428fe796a83</citedby><cites>FETCH-LOGICAL-c471t-688babe6ba905fc038e57834bd7415be167d962fbf7006ebfc55b9428fe796a83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00232-013-9598-8$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00232-013-9598-8$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24121666$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Galizia, Luciano</creatorcontrib><creatorcontrib>Marino, Gabriela I.</creatorcontrib><creatorcontrib>Ojea, Alejandro</creatorcontrib><creatorcontrib>Kotsias, Basilio A.</creatorcontrib><title>Hypotonic Regulation of Mouse Epithelial Sodium Channel in Xenopus laevis Oocytes</title><title>The Journal of membrane biology</title><addtitle>J Membrane Biol</addtitle><addtitle>J Membr Biol</addtitle><description>The regulation of the epithelial Na
+
channel (ENaC) during cell swelling is relevant in cellular processes in which cell volume changes occur, i.e., migration, proliferation and cell absorption. Its sensitivity to hypotonically induced swelling was investigated in the
Xenopus
oocyte expression system with the injection of the three subunits of mouse ENaC. We used voltage-clamp techniques to study the amiloride-sensitive Na
+
currents (
I
Na
(amil)
) and video microscopic methodologies to assess oocyte volume changes. Under conditions of mild swelling (25 % reduced hypotonicity) inward current amplitude decreased rapidly over 1.5 min. In contrast, there was no change in current amplitude of H
2
O-injected oocytes to the osmotic insult.
I
Na
(amil)
kinetics analysis revealed a decrease in the slower inactivation time constant during the hypotonic stimuli. Currents from ENaC-injected oocytes were not sensitive to external Cl
−
reduction. Neither short- nor long-term cytochalasin D treatment affected the observed response. Oocytes expressing a DEG mutant β-ENaC subunit (β-S518K) with an open probability of 1 had reduced
I
Na
(amil)
hypotonic response compared to oocytes injected with wild-type ENaC subunits. Finally, during the hypotonic response ENaC-injected oocytes did not show a cell volume difference compared with water-injected oocytes. On this basis we suggest that hypotonicity-dependent ENaC inhibition is principally mediated through an effect on open probability of channels in the membrane.</description><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Biological Transport</subject><subject>Biomedical and Life Sciences</subject><subject>Cellular biology</subject><subject>Epithelial Sodium Channels - genetics</subject><subject>Epithelial Sodium Channels - metabolism</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Human Physiology</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Membrane Potentials</subject><subject>Membranes</subject><subject>Mice</subject><subject>Oocytes - metabolism</subject><subject>Osmotic Pressure</subject><subject>Rodents</subject><subject>Sodium - metabolism</subject><subject>Xenopus laevis</subject><issn>0022-2631</issn><issn>1432-1424</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkV1LHTEQhoNU9NT2B3gjgd70ZttMNl97KQetgiL2A3oXkj2zGtmTrJvdwvn3zeFYEUF6NTDz5J0JDyHHwL4AY_prZozXvGJQV41sTGX2yAJE6YDg4h1ZlDGvuKrhkLzP-YEx0FqJA3LIBXBQSi3I7cVmSFOKoaXf8W7u3RRSpKmj12nOSM-GMN1jH1xPf6RVmNd0ee9ixJ6GSH9jTMOcae_wT8j0JrWbCfMHst-5PuPHp3pEfp2f_VxeVFc33y6Xp1dVKzRMlTLGO4_Ku4bJrmW1QalNLfxKC5AeQelVo3jnO82YQt-1UvpGcNOhbpQz9RH5vMsdxvQ4Y57sOuQW-95FLLdbkFwIprVR_0eFapSoQcqCfnqFPqR5jOUjhRKmrAYFhYId1Y4p5xE7O4xh7caNBWa3auxOjS1q7FaN3d578pQ8-zWunl_8c1EAvgNyGcU7HF-sfjP1L3MMl_M</recordid><startdate>20131201</startdate><enddate>20131201</enddate><creator>Galizia, Luciano</creator><creator>Marino, Gabriela I.</creator><creator>Ojea, Alejandro</creator><creator>Kotsias, Basilio A.</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>NAPCQ</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>F1W</scope><scope>H95</scope><scope>L.G</scope></search><sort><creationdate>20131201</creationdate><title>Hypotonic Regulation of Mouse Epithelial Sodium Channel in Xenopus laevis Oocytes</title><author>Galizia, Luciano ; Marino, Gabriela I. ; Ojea, Alejandro ; Kotsias, Basilio A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-688babe6ba905fc038e57834bd7415be167d962fbf7006ebfc55b9428fe796a83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Biological Transport</topic><topic>Biomedical and Life Sciences</topic><topic>Cellular biology</topic><topic>Epithelial Sodium Channels - genetics</topic><topic>Epithelial Sodium Channels - metabolism</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Human Physiology</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Membrane Potentials</topic><topic>Membranes</topic><topic>Mice</topic><topic>Oocytes - metabolism</topic><topic>Osmotic Pressure</topic><topic>Rodents</topic><topic>Sodium - metabolism</topic><topic>Xenopus laevis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Galizia, Luciano</creatorcontrib><creatorcontrib>Marino, Gabriela I.</creatorcontrib><creatorcontrib>Ojea, Alejandro</creatorcontrib><creatorcontrib>Kotsias, Basilio A.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nursing & Allied Health Database</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection (ProQuest)</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Materials Science Collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>ASFA: Aquatic Sciences and Fisheries Abstracts</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) 1: Biological Sciences & Living Resources</collection><collection>Aquatic Science & Fisheries Abstracts (ASFA) Professional</collection><jtitle>The Journal of membrane biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Galizia, Luciano</au><au>Marino, Gabriela I.</au><au>Ojea, Alejandro</au><au>Kotsias, Basilio A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hypotonic Regulation of Mouse Epithelial Sodium Channel in Xenopus laevis Oocytes</atitle><jtitle>The Journal of membrane biology</jtitle><stitle>J Membrane Biol</stitle><addtitle>J Membr Biol</addtitle><date>2013-12-01</date><risdate>2013</risdate><volume>246</volume><issue>12</issue><spage>949</spage><epage>958</epage><pages>949-958</pages><issn>0022-2631</issn><eissn>1432-1424</eissn><abstract>The regulation of the epithelial Na
+
channel (ENaC) during cell swelling is relevant in cellular processes in which cell volume changes occur, i.e., migration, proliferation and cell absorption. Its sensitivity to hypotonically induced swelling was investigated in the
Xenopus
oocyte expression system with the injection of the three subunits of mouse ENaC. We used voltage-clamp techniques to study the amiloride-sensitive Na
+
currents (
I
Na
(amil)
) and video microscopic methodologies to assess oocyte volume changes. Under conditions of mild swelling (25 % reduced hypotonicity) inward current amplitude decreased rapidly over 1.5 min. In contrast, there was no change in current amplitude of H
2
O-injected oocytes to the osmotic insult.
I
Na
(amil)
kinetics analysis revealed a decrease in the slower inactivation time constant during the hypotonic stimuli. Currents from ENaC-injected oocytes were not sensitive to external Cl
−
reduction. Neither short- nor long-term cytochalasin D treatment affected the observed response. Oocytes expressing a DEG mutant β-ENaC subunit (β-S518K) with an open probability of 1 had reduced
I
Na
(amil)
hypotonic response compared to oocytes injected with wild-type ENaC subunits. Finally, during the hypotonic response ENaC-injected oocytes did not show a cell volume difference compared with water-injected oocytes. On this basis we suggest that hypotonicity-dependent ENaC inhibition is principally mediated through an effect on open probability of channels in the membrane.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>24121666</pmid><doi>10.1007/s00232-013-9598-8</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actins - metabolism Animals Biochemistry Biological Transport Biomedical and Life Sciences Cellular biology Epithelial Sodium Channels - genetics Epithelial Sodium Channels - metabolism Female Gene Expression Human Physiology Kinetics Life Sciences Membrane Potentials Membranes Mice Oocytes - metabolism Osmotic Pressure Rodents Sodium - metabolism Xenopus laevis |
| title | Hypotonic Regulation of Mouse Epithelial Sodium Channel in Xenopus laevis Oocytes |
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