Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure
Two-pore-domain potassium (K2P) channels modulate cellular excitability. The significance of stretch-activated cardiac K2P channels (K2P2.1, TREK-1, KCNK2; K2P4.1, TRAAK, KCNK4; K2P10.1, TREK-2, KCNK10) in heart disease has not been elucidated in detail. The aim of this work was to assess expression...
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| Veröffentlicht in: | Progress in biophysics and molecular biology 2017-11, Vol.130 (Pt B), p.233-243 |
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| creator | Schmidt, Constanze Wiedmann, Felix Kallenberger, Stefan M. Ratte, Antonius Schulte, Jan S. Scholz, Beatrix Müller, Frank Ulrich Voigt, Niels Zafeiriou, Maria-Patapia Ehrlich, Joachim R. Tochtermann, Ursula Veres, Gábor Ruhparwar, Arjang Karck, Matthias Katus, Hugo A. Thomas, Dierk |
| description | Two-pore-domain potassium (K2P) channels modulate cellular excitability. The significance of stretch-activated cardiac K2P channels (K2P2.1, TREK-1, KCNK2; K2P4.1, TRAAK, KCNK4; K2P10.1, TREK-2, KCNK10) in heart disease has not been elucidated in detail. The aim of this work was to assess expression and remodeling of mechanosensitive K2P channels in atrial fibrillation (AF) and heart failure (HF) patients in comparison to murine models.
Cardiac K2P channel levels were quantified in atrial (A) and ventricular (V) tissue obtained from patients undergoing open heart surgery. In addition, control mice and mouse models of AF (cAMP-response element modulator (CREM)-IbΔC-X transgenic animals) or HF (cardiac dysfunction induced by transverse aortic constriction, TAC) were employed. Human and murine KCNK2 displayed highest mRNA abundance among mechanosensitive members of the K2P channel family (V > A). Disease-associated K2P2.1 remodeling was studied in detail. In patients with impaired left ventricular function, atrial KCNK2 (K2P2.1) mRNA and protein expression was significantly reduced. In AF subjects, downregulation of atrial and ventricular KCNK2 (K2P2.1) mRNA and protein levels was observed. AF-associated suppression of atrial Kcnk2 (K2P2.1) mRNA and protein was recapitulated in CREM-transgenic mice. Ventricular Kcnk2 expression was not significantly altered in mouse models of disease.
In conclusion, mechanosensitive K2P2.1 and K2P10.1 K+ channels are expressed throughout the heart. HF- and AF-associated downregulation of KCNK2 (K2P2.1) mRNA and protein levels suggest a mechanistic contribution to cardiac arrhythmogenesis. |
| doi_str_mv | 10.1016/j.pbiomolbio.2017.05.004 |
| format | Article |
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Cardiac K2P channel levels were quantified in atrial (A) and ventricular (V) tissue obtained from patients undergoing open heart surgery. In addition, control mice and mouse models of AF (cAMP-response element modulator (CREM)-IbΔC-X transgenic animals) or HF (cardiac dysfunction induced by transverse aortic constriction, TAC) were employed. Human and murine KCNK2 displayed highest mRNA abundance among mechanosensitive members of the K2P channel family (V > A). Disease-associated K2P2.1 remodeling was studied in detail. In patients with impaired left ventricular function, atrial KCNK2 (K2P2.1) mRNA and protein expression was significantly reduced. In AF subjects, downregulation of atrial and ventricular KCNK2 (K2P2.1) mRNA and protein levels was observed. AF-associated suppression of atrial Kcnk2 (K2P2.1) mRNA and protein was recapitulated in CREM-transgenic mice. Ventricular Kcnk2 expression was not significantly altered in mouse models of disease.
In conclusion, mechanosensitive K2P2.1 and K2P10.1 K+ channels are expressed throughout the heart. HF- and AF-associated downregulation of KCNK2 (K2P2.1) mRNA and protein levels suggest a mechanistic contribution to cardiac arrhythmogenesis.</description><identifier>ISSN: 0079-6107</identifier><identifier>EISSN: 1873-1732</identifier><identifier>DOI: 10.1016/j.pbiomolbio.2017.05.004</identifier><identifier>PMID: 28526353</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Aged ; Atrial fibrillation ; Atrial Fibrillation - genetics ; Atrial Fibrillation - metabolism ; Biomechanical Phenomena ; Down-Regulation ; Female ; Heart failure ; Heart Failure - genetics ; Heart Failure - metabolism ; Humans ; Male ; Mechanical Phenomena ; Middle Aged ; Models, Molecular ; Myocardium - metabolism ; Potassium Channels, Tandem Pore Domain - chemistry ; Potassium Channels, Tandem Pore Domain - genetics ; Potassium Channels, Tandem Pore Domain - metabolism ; Protein Conformation ; Protein Transport ; Stretch-activated ion channels ; TREK-1 ; Two-pore-domain potassium channels ; Up-Regulation</subject><ispartof>Progress in biophysics and molecular biology, 2017-11, Vol.130 (Pt B), p.233-243</ispartof><rights>2017 Elsevier Ltd</rights><rights>Copyright © 2017 Elsevier Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c374t-9f3a62ed0170248cda9fe7a09c3081635de87ec17f9f4c498137acb1308bd68d3</citedby><cites>FETCH-LOGICAL-c374t-9f3a62ed0170248cda9fe7a09c3081635de87ec17f9f4c498137acb1308bd68d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0079610717300287$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28526353$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Schmidt, Constanze</creatorcontrib><creatorcontrib>Wiedmann, Felix</creatorcontrib><creatorcontrib>Kallenberger, Stefan M.</creatorcontrib><creatorcontrib>Ratte, Antonius</creatorcontrib><creatorcontrib>Schulte, Jan S.</creatorcontrib><creatorcontrib>Scholz, Beatrix</creatorcontrib><creatorcontrib>Müller, Frank Ulrich</creatorcontrib><creatorcontrib>Voigt, Niels</creatorcontrib><creatorcontrib>Zafeiriou, Maria-Patapia</creatorcontrib><creatorcontrib>Ehrlich, Joachim R.</creatorcontrib><creatorcontrib>Tochtermann, Ursula</creatorcontrib><creatorcontrib>Veres, Gábor</creatorcontrib><creatorcontrib>Ruhparwar, Arjang</creatorcontrib><creatorcontrib>Karck, Matthias</creatorcontrib><creatorcontrib>Katus, Hugo A.</creatorcontrib><creatorcontrib>Thomas, Dierk</creatorcontrib><title>Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure</title><title>Progress in biophysics and molecular biology</title><addtitle>Prog Biophys Mol Biol</addtitle><description>Two-pore-domain potassium (K2P) channels modulate cellular excitability. The significance of stretch-activated cardiac K2P channels (K2P2.1, TREK-1, KCNK2; K2P4.1, TRAAK, KCNK4; K2P10.1, TREK-2, KCNK10) in heart disease has not been elucidated in detail. The aim of this work was to assess expression and remodeling of mechanosensitive K2P channels in atrial fibrillation (AF) and heart failure (HF) patients in comparison to murine models.
Cardiac K2P channel levels were quantified in atrial (A) and ventricular (V) tissue obtained from patients undergoing open heart surgery. In addition, control mice and mouse models of AF (cAMP-response element modulator (CREM)-IbΔC-X transgenic animals) or HF (cardiac dysfunction induced by transverse aortic constriction, TAC) were employed. Human and murine KCNK2 displayed highest mRNA abundance among mechanosensitive members of the K2P channel family (V > A). Disease-associated K2P2.1 remodeling was studied in detail. In patients with impaired left ventricular function, atrial KCNK2 (K2P2.1) mRNA and protein expression was significantly reduced. In AF subjects, downregulation of atrial and ventricular KCNK2 (K2P2.1) mRNA and protein levels was observed. AF-associated suppression of atrial Kcnk2 (K2P2.1) mRNA and protein was recapitulated in CREM-transgenic mice. Ventricular Kcnk2 expression was not significantly altered in mouse models of disease.
In conclusion, mechanosensitive K2P2.1 and K2P10.1 K+ channels are expressed throughout the heart. HF- and AF-associated downregulation of KCNK2 (K2P2.1) mRNA and protein levels suggest a mechanistic contribution to cardiac arrhythmogenesis.</description><subject>Aged</subject><subject>Atrial fibrillation</subject><subject>Atrial Fibrillation - genetics</subject><subject>Atrial Fibrillation - metabolism</subject><subject>Biomechanical Phenomena</subject><subject>Down-Regulation</subject><subject>Female</subject><subject>Heart failure</subject><subject>Heart Failure - genetics</subject><subject>Heart Failure - metabolism</subject><subject>Humans</subject><subject>Male</subject><subject>Mechanical Phenomena</subject><subject>Middle Aged</subject><subject>Models, Molecular</subject><subject>Myocardium - metabolism</subject><subject>Potassium Channels, Tandem Pore Domain - chemistry</subject><subject>Potassium Channels, Tandem Pore Domain - genetics</subject><subject>Potassium Channels, Tandem Pore Domain - metabolism</subject><subject>Protein Conformation</subject><subject>Protein Transport</subject><subject>Stretch-activated ion channels</subject><subject>TREK-1</subject><subject>Two-pore-domain potassium channels</subject><subject>Up-Regulation</subject><issn>0079-6107</issn><issn>1873-1732</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1v1DAQQC0EokvhLyAfyyFhbCexww0qWhCVqFQ4W4490XqVxMF2WvHv69UWOHLxSJ43X48QyqBmwLr3h3odfJjDVN6aA5M1tDVA84zsmJKiYlLw52QHIPuqYyDPyKuUDgDAmexekjOuWt6JVuzIw12OmO2-Mjb7e5PR0fwQqjVErFyYjV_oxTd--46uIZuU_DZTuzfLglOiJZf3SPdoYv5Ar4LdEg0LNTl6M9HRD9FPk8n--Le4E0dH46ct4mvyYjRTwjdP8Zz8vPr84_JLdfP9-uvlx5vKCtnkqh-F6Ti6ciLwRlln-hGlgd4KUKyc4FBJtEyO_djYpldMSGMHVrKD65QT5-Ti1HeN4deGKevZJ4tlrwXDljTrAZTgLRMFVSfUxpBSxFGv0c8m_tYM9FG7Puh_2vVRu4ZWF-2l9O3TlG2Y0f0t_OO5AJ9OQPGG9x6jTtbjYtH5iDZrF_z_pzwCkyGaEA</recordid><startdate>201711</startdate><enddate>201711</enddate><creator>Schmidt, Constanze</creator><creator>Wiedmann, Felix</creator><creator>Kallenberger, Stefan M.</creator><creator>Ratte, Antonius</creator><creator>Schulte, Jan S.</creator><creator>Scholz, Beatrix</creator><creator>Müller, Frank Ulrich</creator><creator>Voigt, Niels</creator><creator>Zafeiriou, Maria-Patapia</creator><creator>Ehrlich, Joachim R.</creator><creator>Tochtermann, Ursula</creator><creator>Veres, Gábor</creator><creator>Ruhparwar, Arjang</creator><creator>Karck, Matthias</creator><creator>Katus, Hugo A.</creator><creator>Thomas, Dierk</creator><general>Elsevier Ltd</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></search><sort><creationdate>201711</creationdate><title>Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure</title><author>Schmidt, Constanze ; Wiedmann, Felix ; Kallenberger, Stefan M. ; Ratte, Antonius ; Schulte, Jan S. ; Scholz, Beatrix ; Müller, Frank Ulrich ; Voigt, Niels ; Zafeiriou, Maria-Patapia ; Ehrlich, Joachim R. ; Tochtermann, Ursula ; Veres, Gábor ; Ruhparwar, Arjang ; Karck, Matthias ; Katus, Hugo A. ; Thomas, Dierk</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c374t-9f3a62ed0170248cda9fe7a09c3081635de87ec17f9f4c498137acb1308bd68d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Aged</topic><topic>Atrial fibrillation</topic><topic>Atrial Fibrillation - genetics</topic><topic>Atrial Fibrillation - metabolism</topic><topic>Biomechanical Phenomena</topic><topic>Down-Regulation</topic><topic>Female</topic><topic>Heart failure</topic><topic>Heart Failure - genetics</topic><topic>Heart Failure - metabolism</topic><topic>Humans</topic><topic>Male</topic><topic>Mechanical Phenomena</topic><topic>Middle Aged</topic><topic>Models, Molecular</topic><topic>Myocardium - metabolism</topic><topic>Potassium Channels, Tandem Pore Domain - chemistry</topic><topic>Potassium Channels, Tandem Pore Domain - genetics</topic><topic>Potassium Channels, Tandem Pore Domain - metabolism</topic><topic>Protein Conformation</topic><topic>Protein Transport</topic><topic>Stretch-activated ion channels</topic><topic>TREK-1</topic><topic>Two-pore-domain potassium channels</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Schmidt, Constanze</creatorcontrib><creatorcontrib>Wiedmann, Felix</creatorcontrib><creatorcontrib>Kallenberger, Stefan M.</creatorcontrib><creatorcontrib>Ratte, Antonius</creatorcontrib><creatorcontrib>Schulte, Jan S.</creatorcontrib><creatorcontrib>Scholz, Beatrix</creatorcontrib><creatorcontrib>Müller, Frank Ulrich</creatorcontrib><creatorcontrib>Voigt, Niels</creatorcontrib><creatorcontrib>Zafeiriou, Maria-Patapia</creatorcontrib><creatorcontrib>Ehrlich, Joachim R.</creatorcontrib><creatorcontrib>Tochtermann, Ursula</creatorcontrib><creatorcontrib>Veres, Gábor</creatorcontrib><creatorcontrib>Ruhparwar, Arjang</creatorcontrib><creatorcontrib>Karck, Matthias</creatorcontrib><creatorcontrib>Katus, Hugo A.</creatorcontrib><creatorcontrib>Thomas, Dierk</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><jtitle>Progress in biophysics and molecular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Schmidt, Constanze</au><au>Wiedmann, Felix</au><au>Kallenberger, Stefan M.</au><au>Ratte, Antonius</au><au>Schulte, Jan S.</au><au>Scholz, Beatrix</au><au>Müller, Frank Ulrich</au><au>Voigt, Niels</au><au>Zafeiriou, Maria-Patapia</au><au>Ehrlich, Joachim R.</au><au>Tochtermann, Ursula</au><au>Veres, Gábor</au><au>Ruhparwar, Arjang</au><au>Karck, Matthias</au><au>Katus, Hugo A.</au><au>Thomas, Dierk</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure</atitle><jtitle>Progress in biophysics and molecular biology</jtitle><addtitle>Prog Biophys Mol Biol</addtitle><date>2017-11</date><risdate>2017</risdate><volume>130</volume><issue>Pt B</issue><spage>233</spage><epage>243</epage><pages>233-243</pages><issn>0079-6107</issn><eissn>1873-1732</eissn><abstract>Two-pore-domain potassium (K2P) channels modulate cellular excitability. The significance of stretch-activated cardiac K2P channels (K2P2.1, TREK-1, KCNK2; K2P4.1, TRAAK, KCNK4; K2P10.1, TREK-2, KCNK10) in heart disease has not been elucidated in detail. The aim of this work was to assess expression and remodeling of mechanosensitive K2P channels in atrial fibrillation (AF) and heart failure (HF) patients in comparison to murine models.
Cardiac K2P channel levels were quantified in atrial (A) and ventricular (V) tissue obtained from patients undergoing open heart surgery. In addition, control mice and mouse models of AF (cAMP-response element modulator (CREM)-IbΔC-X transgenic animals) or HF (cardiac dysfunction induced by transverse aortic constriction, TAC) were employed. Human and murine KCNK2 displayed highest mRNA abundance among mechanosensitive members of the K2P channel family (V > A). Disease-associated K2P2.1 remodeling was studied in detail. In patients with impaired left ventricular function, atrial KCNK2 (K2P2.1) mRNA and protein expression was significantly reduced. In AF subjects, downregulation of atrial and ventricular KCNK2 (K2P2.1) mRNA and protein levels was observed. AF-associated suppression of atrial Kcnk2 (K2P2.1) mRNA and protein was recapitulated in CREM-transgenic mice. Ventricular Kcnk2 expression was not significantly altered in mouse models of disease.
In conclusion, mechanosensitive K2P2.1 and K2P10.1 K+ channels are expressed throughout the heart. HF- and AF-associated downregulation of KCNK2 (K2P2.1) mRNA and protein levels suggest a mechanistic contribution to cardiac arrhythmogenesis.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>28526353</pmid><doi>10.1016/j.pbiomolbio.2017.05.004</doi><tpages>11</tpages></addata></record> |
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| subjects | Aged Atrial fibrillation Atrial Fibrillation - genetics Atrial Fibrillation - metabolism Biomechanical Phenomena Down-Regulation Female Heart failure Heart Failure - genetics Heart Failure - metabolism Humans Male Mechanical Phenomena Middle Aged Models, Molecular Myocardium - metabolism Potassium Channels, Tandem Pore Domain - chemistry Potassium Channels, Tandem Pore Domain - genetics Potassium Channels, Tandem Pore Domain - metabolism Protein Conformation Protein Transport Stretch-activated ion channels TREK-1 Two-pore-domain potassium channels Up-Regulation |
| title | Stretch-activated two-pore-domain (K2P) potassium channels in the heart: Focus on atrial fibrillation and heart failure |
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