ANO1 contributes to Angiotensin-II-activated Ca2+-dependent Cl− current in human atrial fibroblasts
Cardiac fibroblasts are an integral part of the myocardial tissue and contribute to its remodelling. This study characterises for the first time the calcium-dependent chloride channels (CaCC) in the plasma membrane of primary human atrial cardiac fibroblasts by means of the iodide efflux and the pat...
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| Veröffentlicht in: | Journal of molecular and cellular cardiology 2014-03, Vol.68, p.12-19 |
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| creator | El Chemaly, Antoun Norez, Caroline Magaud, Christophe Bescond, Jocelyn Chatelier, Aurelien Fares, Nassim Findlay, Ian Jayle, Christophe Becq, Frederic Faivre, Jean-François Bois, Patrick |
| description | Cardiac fibroblasts are an integral part of the myocardial tissue and contribute to its remodelling. This study characterises for the first time the calcium-dependent chloride channels (CaCC) in the plasma membrane of primary human atrial cardiac fibroblasts by means of the iodide efflux and the patch clamp methods. The calcium ionophore A23187 and Angiotensin II (Ang II) activate a chloride conductance in cardiac fibroblasts that shares pharmacological similarities with calcium-dependent chloride channels. This chloride conductance is depressed by RNAi-mediated selective Anoctamine 1 (ANO1) but not by Anoctamine 2 (ANO2) which has been revealed as CaCC and is inhibited by the selective ANO1 inhibitor, T16inh-A01. The effect of Ang II on anion efflux is mediated through AT1 receptors (with an EC50=13.8±1.3nM). The decrease of anion efflux by calphostin C and bisindolylmaleimide I (BIM I) suggests that chloride conductance activation is dependent on PKC. We conclude that ANO1 contributes to CaCC current in human cardiac fibroblasts and that this is regulated by Ang II acting via the AT1 receptor pathway.
•ANO1 carries CaCC current in human cardiac fibroblasts.•ANO1 is regulated by Ang II via the AT1 receptor pathway.•ANO1 may influence cardiac fibroblast proliferation and secretion of collagen.•ANO1 may regulate hypertrophy and fibrosis resulting from ischemia. |
| doi_str_mv | 10.1016/j.yjmcc.2013.12.027 |
| format | Article |
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•ANO1 carries CaCC current in human cardiac fibroblasts.•ANO1 is regulated by Ang II via the AT1 receptor pathway.•ANO1 may influence cardiac fibroblast proliferation and secretion of collagen.•ANO1 may regulate hypertrophy and fibrosis resulting from ischemia.</description><identifier>ISSN: 0022-2828</identifier><identifier>EISSN: 1095-8584</identifier><identifier>DOI: 10.1016/j.yjmcc.2013.12.027</identifier><identifier>PMID: 24412532</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Aged ; Angiotensin II ; Angiotensin II - physiology ; ANO1 ; Anoctamin-1 ; Biological Transport ; Calcium Signaling ; Calcium-dependent chloride channels ; Cell Membrane - metabolism ; Cells, Cultured ; Chloride Channels - physiology ; Chlorides - metabolism ; Female ; Fibroblasts - metabolism ; Heart Atria - cytology ; Human cardiac fibroblasts ; Humans ; Kinetics ; Life Sciences ; Male ; Neoplasm Proteins - physiology ; Receptor, Angiotensin, Type 1 - metabolism ; TMEM16A</subject><ispartof>Journal of molecular and cellular cardiology, 2014-03, Vol.68, p.12-19</ispartof><rights>2014 Elsevier Ltd</rights><rights>Copyright © 2014 Elsevier Ltd. All rights reserved.</rights><rights>Distributed under a Creative Commons Attribution 4.0 International License</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c323t-e799fc46ac2c47cc1f2d3473f12ba76e0399c12bfb2db658e91d407baa56bd5e3</citedby><cites>FETCH-LOGICAL-c323t-e799fc46ac2c47cc1f2d3473f12ba76e0399c12bfb2db658e91d407baa56bd5e3</cites><orcidid>0000-0002-7441-1182 ; 0000-0003-3915-0973 ; 0000-0003-0605-1880 ; 0000-0002-2935-2611 ; 0000-0002-8995-9052 ; 0000-0002-8153-0171 ; 0000-0002-5129-2723</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0022282814000054$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>230,314,776,780,881,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24412532$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.science/hal-00990329$$DView record in HAL$$Hfree_for_read</backlink></links><search><creatorcontrib>El Chemaly, Antoun</creatorcontrib><creatorcontrib>Norez, Caroline</creatorcontrib><creatorcontrib>Magaud, Christophe</creatorcontrib><creatorcontrib>Bescond, Jocelyn</creatorcontrib><creatorcontrib>Chatelier, Aurelien</creatorcontrib><creatorcontrib>Fares, Nassim</creatorcontrib><creatorcontrib>Findlay, Ian</creatorcontrib><creatorcontrib>Jayle, Christophe</creatorcontrib><creatorcontrib>Becq, Frederic</creatorcontrib><creatorcontrib>Faivre, Jean-François</creatorcontrib><creatorcontrib>Bois, Patrick</creatorcontrib><title>ANO1 contributes to Angiotensin-II-activated Ca2+-dependent Cl− current in human atrial fibroblasts</title><title>Journal of molecular and cellular cardiology</title><addtitle>J Mol Cell Cardiol</addtitle><description>Cardiac fibroblasts are an integral part of the myocardial tissue and contribute to its remodelling. This study characterises for the first time the calcium-dependent chloride channels (CaCC) in the plasma membrane of primary human atrial cardiac fibroblasts by means of the iodide efflux and the patch clamp methods. The calcium ionophore A23187 and Angiotensin II (Ang II) activate a chloride conductance in cardiac fibroblasts that shares pharmacological similarities with calcium-dependent chloride channels. This chloride conductance is depressed by RNAi-mediated selective Anoctamine 1 (ANO1) but not by Anoctamine 2 (ANO2) which has been revealed as CaCC and is inhibited by the selective ANO1 inhibitor, T16inh-A01. The effect of Ang II on anion efflux is mediated through AT1 receptors (with an EC50=13.8±1.3nM). The decrease of anion efflux by calphostin C and bisindolylmaleimide I (BIM I) suggests that chloride conductance activation is dependent on PKC. We conclude that ANO1 contributes to CaCC current in human cardiac fibroblasts and that this is regulated by Ang II acting via the AT1 receptor pathway.
•ANO1 carries CaCC current in human cardiac fibroblasts.•ANO1 is regulated by Ang II via the AT1 receptor pathway.•ANO1 may influence cardiac fibroblast proliferation and secretion of collagen.•ANO1 may regulate hypertrophy and fibrosis resulting from ischemia.</description><subject>Aged</subject><subject>Angiotensin II</subject><subject>Angiotensin II - physiology</subject><subject>ANO1</subject><subject>Anoctamin-1</subject><subject>Biological Transport</subject><subject>Calcium Signaling</subject><subject>Calcium-dependent chloride channels</subject><subject>Cell Membrane - metabolism</subject><subject>Cells, Cultured</subject><subject>Chloride Channels - physiology</subject><subject>Chlorides - metabolism</subject><subject>Female</subject><subject>Fibroblasts - metabolism</subject><subject>Heart Atria - cytology</subject><subject>Human cardiac fibroblasts</subject><subject>Humans</subject><subject>Kinetics</subject><subject>Life Sciences</subject><subject>Male</subject><subject>Neoplasm Proteins - physiology</subject><subject>Receptor, Angiotensin, Type 1 - metabolism</subject><subject>TMEM16A</subject><issn>0022-2828</issn><issn>1095-8584</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kctuEzEUhi0EoqHwBEjIS1A1g3081wWLKKI0UkQ3sLZ8OUMdzdjB9kTqG7DmEXkSJk3pktW56Dv_kf6fkLeclZzx5uO-vN9PxpTAuCg5lAzaZ2TFWV8XXd1Vz8mKMYACOuguyKuU9oyxvhLiJbmAquJQC1gRXH-95dQEn6PTc8ZEc6Br_8OFjD45X2y3hTLZHVVGSzcKrgqLB_QWfaab8c-v39TMMZ4m5-ndPClP1aKlRjo4HYMeVcrpNXkxqDHhm8d6Sb5ff_62uSl2t1-2m_WuMAJELrDt-8FUjTJgqtYYPoAVVSsGDlq1DTLR92bpBw1WN3WHPbcVa7VSdaNtjeKSfDjr3qlRHqKbVLyXQTl5s97J025xoGcC-iNf2Pdn9hDDzxlTlpNLBsdReQxzkrxmvBNtA-2CijNqYkgp4vCkzZk8ZSH38iELecpCcpDs4erd44NZT2ifbv6ZvwCfzgAulhwdRpmMQ2_QuogmSxvcfx_8BT_Um-o</recordid><startdate>201403</startdate><enddate>201403</enddate><creator>El Chemaly, Antoun</creator><creator>Norez, Caroline</creator><creator>Magaud, Christophe</creator><creator>Bescond, Jocelyn</creator><creator>Chatelier, Aurelien</creator><creator>Fares, Nassim</creator><creator>Findlay, Ian</creator><creator>Jayle, Christophe</creator><creator>Becq, Frederic</creator><creator>Faivre, Jean-François</creator><creator>Bois, Patrick</creator><general>Elsevier Ltd</general><general>Elsevier</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>7X8</scope><scope>1XC</scope><orcidid>https://orcid.org/0000-0002-7441-1182</orcidid><orcidid>https://orcid.org/0000-0003-3915-0973</orcidid><orcidid>https://orcid.org/0000-0003-0605-1880</orcidid><orcidid>https://orcid.org/0000-0002-2935-2611</orcidid><orcidid>https://orcid.org/0000-0002-8995-9052</orcidid><orcidid>https://orcid.org/0000-0002-8153-0171</orcidid><orcidid>https://orcid.org/0000-0002-5129-2723</orcidid></search><sort><creationdate>201403</creationdate><title>ANO1 contributes to Angiotensin-II-activated Ca2+-dependent Cl− current in human atrial fibroblasts</title><author>El Chemaly, Antoun ; Norez, Caroline ; Magaud, Christophe ; Bescond, Jocelyn ; Chatelier, Aurelien ; Fares, Nassim ; Findlay, Ian ; Jayle, Christophe ; Becq, Frederic ; Faivre, Jean-François ; Bois, Patrick</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c323t-e799fc46ac2c47cc1f2d3473f12ba76e0399c12bfb2db658e91d407baa56bd5e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Aged</topic><topic>Angiotensin II</topic><topic>Angiotensin II - physiology</topic><topic>ANO1</topic><topic>Anoctamin-1</topic><topic>Biological Transport</topic><topic>Calcium Signaling</topic><topic>Calcium-dependent chloride channels</topic><topic>Cell Membrane - metabolism</topic><topic>Cells, Cultured</topic><topic>Chloride Channels - physiology</topic><topic>Chlorides - metabolism</topic><topic>Female</topic><topic>Fibroblasts - metabolism</topic><topic>Heart Atria - cytology</topic><topic>Human cardiac fibroblasts</topic><topic>Humans</topic><topic>Kinetics</topic><topic>Life Sciences</topic><topic>Male</topic><topic>Neoplasm Proteins - physiology</topic><topic>Receptor, Angiotensin, Type 1 - metabolism</topic><topic>TMEM16A</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>El Chemaly, Antoun</creatorcontrib><creatorcontrib>Norez, Caroline</creatorcontrib><creatorcontrib>Magaud, Christophe</creatorcontrib><creatorcontrib>Bescond, Jocelyn</creatorcontrib><creatorcontrib>Chatelier, Aurelien</creatorcontrib><creatorcontrib>Fares, Nassim</creatorcontrib><creatorcontrib>Findlay, Ian</creatorcontrib><creatorcontrib>Jayle, Christophe</creatorcontrib><creatorcontrib>Becq, Frederic</creatorcontrib><creatorcontrib>Faivre, Jean-François</creatorcontrib><creatorcontrib>Bois, Patrick</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><jtitle>Journal of molecular and cellular cardiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>El Chemaly, Antoun</au><au>Norez, Caroline</au><au>Magaud, Christophe</au><au>Bescond, Jocelyn</au><au>Chatelier, Aurelien</au><au>Fares, Nassim</au><au>Findlay, Ian</au><au>Jayle, Christophe</au><au>Becq, Frederic</au><au>Faivre, Jean-François</au><au>Bois, Patrick</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ANO1 contributes to Angiotensin-II-activated Ca2+-dependent Cl− current in human atrial fibroblasts</atitle><jtitle>Journal of molecular and cellular cardiology</jtitle><addtitle>J Mol Cell Cardiol</addtitle><date>2014-03</date><risdate>2014</risdate><volume>68</volume><spage>12</spage><epage>19</epage><pages>12-19</pages><issn>0022-2828</issn><eissn>1095-8584</eissn><abstract>Cardiac fibroblasts are an integral part of the myocardial tissue and contribute to its remodelling. This study characterises for the first time the calcium-dependent chloride channels (CaCC) in the plasma membrane of primary human atrial cardiac fibroblasts by means of the iodide efflux and the patch clamp methods. The calcium ionophore A23187 and Angiotensin II (Ang II) activate a chloride conductance in cardiac fibroblasts that shares pharmacological similarities with calcium-dependent chloride channels. This chloride conductance is depressed by RNAi-mediated selective Anoctamine 1 (ANO1) but not by Anoctamine 2 (ANO2) which has been revealed as CaCC and is inhibited by the selective ANO1 inhibitor, T16inh-A01. The effect of Ang II on anion efflux is mediated through AT1 receptors (with an EC50=13.8±1.3nM). The decrease of anion efflux by calphostin C and bisindolylmaleimide I (BIM I) suggests that chloride conductance activation is dependent on PKC. We conclude that ANO1 contributes to CaCC current in human cardiac fibroblasts and that this is regulated by Ang II acting via the AT1 receptor pathway.
•ANO1 carries CaCC current in human cardiac fibroblasts.•ANO1 is regulated by Ang II via the AT1 receptor pathway.•ANO1 may influence cardiac fibroblast proliferation and secretion of collagen.•ANO1 may regulate hypertrophy and fibrosis resulting from ischemia.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>24412532</pmid><doi>10.1016/j.yjmcc.2013.12.027</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0002-7441-1182</orcidid><orcidid>https://orcid.org/0000-0003-3915-0973</orcidid><orcidid>https://orcid.org/0000-0003-0605-1880</orcidid><orcidid>https://orcid.org/0000-0002-2935-2611</orcidid><orcidid>https://orcid.org/0000-0002-8995-9052</orcidid><orcidid>https://orcid.org/0000-0002-8153-0171</orcidid><orcidid>https://orcid.org/0000-0002-5129-2723</orcidid></addata></record> |
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| subjects | Aged Angiotensin II Angiotensin II - physiology ANO1 Anoctamin-1 Biological Transport Calcium Signaling Calcium-dependent chloride channels Cell Membrane - metabolism Cells, Cultured Chloride Channels - physiology Chlorides - metabolism Female Fibroblasts - metabolism Heart Atria - cytology Human cardiac fibroblasts Humans Kinetics Life Sciences Male Neoplasm Proteins - physiology Receptor, Angiotensin, Type 1 - metabolism TMEM16A |
| title | ANO1 contributes to Angiotensin-II-activated Ca2+-dependent Cl− current in human atrial fibroblasts |
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