Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure
We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca 2+ sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the...
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| Veröffentlicht in: | Basic research in cardiology 2012-03, Vol.107 (2), p.244-244, Article 244 |
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| creator | Czuriga, Dániel Tóth, Attila Pásztor, Enikő T. Balogh, Ágnes Bodnár, Andrea Nizsalóczki, Enikő Lionetti, Vincenzo Recchia, Fabio A. Czuriga, István Édes, István Papp, Zoltán |
| description | We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca
2+
sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation was wider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42;
P
= 0.0047) or that of the free wall of the control animals (IQR = 0.36;
P
= 0.0093). Additionally, the Ca
2+
sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca
2+
sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF. |
| doi_str_mv | 10.1007/s00395-012-0244-x |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3329882</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2606195501</sourcerecordid><originalsourceid>FETCH-LOGICAL-c468t-9c85b81df74294b64f53cf9937ba6a21a92f8153fcbace1715637d4a9eeeaa983</originalsourceid><addsrcrecordid>eNp1kUtv3CAUhVHVqpmm_QHdVKibrmh52YZNpWrUR6RI2SRrdI1hhsgDLthR5t8Xa9L0IWWBLuh898DlIPSW0Y-M0u5ToVTohlDGCeVSkvtnaMOkaAhTVDxHGyooJUpydYZelXJLKZNty16iM8656NqGbVDYunEkcyK2VnwHOUAfxjAfcYh4zmlKsW4u8LRPpa58HGEOKa4q4CllG6LDhzS4ESePJ6jnHQlxWKwb8N5BnrGHMC7ZvUYvPIzFvXmo5-jm29fr7Q9yefX9YvvlkljZqploq5pescF3kmvZt9I3wnqtRddDC5yB5l6xRnjbg3WsY00rukGCds4BaCXO0eeT77T0BzdYF-cMo5lyOEA-mgTB_KvEsDe7dGeE4FopXg0-PBjk9HNxZTaHUNbvgejSUozmlPOuoSv5_j_yNi051ukq1FFaJ9AVYifI5lRKdv7xKYyaNUZzitHUGM0ao7mvPe_-nuGx43duFeAnoFQp7lz-c_PTrr8AN1qq1w</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>927004299</pqid></control><display><type>article</type><title>Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Czuriga, Dániel ; Tóth, Attila ; Pásztor, Enikő T. ; Balogh, Ágnes ; Bodnár, Andrea ; Nizsalóczki, Enikő ; Lionetti, Vincenzo ; Recchia, Fabio A. ; Czuriga, István ; Édes, István ; Papp, Zoltán</creator><creatorcontrib>Czuriga, Dániel ; Tóth, Attila ; Pásztor, Enikő T. ; Balogh, Ágnes ; Bodnár, Andrea ; Nizsalóczki, Enikő ; Lionetti, Vincenzo ; Recchia, Fabio A. ; Czuriga, István ; Édes, István ; Papp, Zoltán</creatorcontrib><description>We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca
2+
sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation was wider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42;
P
= 0.0047) or that of the free wall of the control animals (IQR = 0.36;
P
= 0.0093). Additionally, the Ca
2+
sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca
2+
sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.</description><identifier>ISSN: 0300-8428</identifier><identifier>EISSN: 1435-1803</identifier><identifier>DOI: 10.1007/s00395-012-0244-x</identifier><identifier>PMID: 22237651</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer-Verlag</publisher><subject>Animals ; Blotting, Western ; Cardiac Pacing, Artificial ; Cardiology ; Cell Separation ; Disease Models, Animal ; Flow Cytometry ; Heart Failure - metabolism ; Immunohistochemistry ; Male ; Medicine ; Medicine & Public Health ; Myofibrils - metabolism ; Original Contribution ; Phosphorylation ; Swine ; Troponin I - metabolism</subject><ispartof>Basic research in cardiology, 2012-03, Vol.107 (2), p.244-244, Article 244</ispartof><rights>The Author(s) 2012</rights><rights>Springer-Verlag 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c468t-9c85b81df74294b64f53cf9937ba6a21a92f8153fcbace1715637d4a9eeeaa983</citedby><cites>FETCH-LOGICAL-c468t-9c85b81df74294b64f53cf9937ba6a21a92f8153fcbace1715637d4a9eeeaa983</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/s00395-012-0244-x$$EPDF$$P50$$Gspringer$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00395-012-0244-x$$EHTML$$P50$$Gspringer$$Hfree_for_read</linktohtml><link.rule.ids>230,314,778,782,883,27913,27914,41477,42546,51308</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22237651$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Czuriga, Dániel</creatorcontrib><creatorcontrib>Tóth, Attila</creatorcontrib><creatorcontrib>Pásztor, Enikő T.</creatorcontrib><creatorcontrib>Balogh, Ágnes</creatorcontrib><creatorcontrib>Bodnár, Andrea</creatorcontrib><creatorcontrib>Nizsalóczki, Enikő</creatorcontrib><creatorcontrib>Lionetti, Vincenzo</creatorcontrib><creatorcontrib>Recchia, Fabio A.</creatorcontrib><creatorcontrib>Czuriga, István</creatorcontrib><creatorcontrib>Édes, István</creatorcontrib><creatorcontrib>Papp, Zoltán</creatorcontrib><title>Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure</title><title>Basic research in cardiology</title><addtitle>Basic Res Cardiol</addtitle><addtitle>Basic Res Cardiol</addtitle><description>We tested the hypothesis that myocardial contractile protein phosphorylation and the Ca
2+
sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation was wider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42;
P
= 0.0047) or that of the free wall of the control animals (IQR = 0.36;
P
= 0.0093). Additionally, the Ca
2+
sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca
2+
sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.</description><subject>Animals</subject><subject>Blotting, Western</subject><subject>Cardiac Pacing, Artificial</subject><subject>Cardiology</subject><subject>Cell Separation</subject><subject>Disease Models, Animal</subject><subject>Flow Cytometry</subject><subject>Heart Failure - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Myofibrils - metabolism</subject><subject>Original Contribution</subject><subject>Phosphorylation</subject><subject>Swine</subject><subject>Troponin I - metabolism</subject><issn>0300-8428</issn><issn>1435-1803</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp1kUtv3CAUhVHVqpmm_QHdVKibrmh52YZNpWrUR6RI2SRrdI1hhsgDLthR5t8Xa9L0IWWBLuh898DlIPSW0Y-M0u5ToVTohlDGCeVSkvtnaMOkaAhTVDxHGyooJUpydYZelXJLKZNty16iM8656NqGbVDYunEkcyK2VnwHOUAfxjAfcYh4zmlKsW4u8LRPpa58HGEOKa4q4CllG6LDhzS4ESePJ6jnHQlxWKwb8N5BnrGHMC7ZvUYvPIzFvXmo5-jm29fr7Q9yefX9YvvlkljZqploq5pescF3kmvZt9I3wnqtRddDC5yB5l6xRnjbg3WsY00rukGCds4BaCXO0eeT77T0BzdYF-cMo5lyOEA-mgTB_KvEsDe7dGeE4FopXg0-PBjk9HNxZTaHUNbvgejSUozmlPOuoSv5_j_yNi051ukq1FFaJ9AVYifI5lRKdv7xKYyaNUZzitHUGM0ao7mvPe_-nuGx43duFeAnoFQp7lz-c_PTrr8AN1qq1w</recordid><startdate>20120301</startdate><enddate>20120301</enddate><creator>Czuriga, Dániel</creator><creator>Tóth, Attila</creator><creator>Pásztor, Enikő T.</creator><creator>Balogh, Ágnes</creator><creator>Bodnár, Andrea</creator><creator>Nizsalóczki, Enikő</creator><creator>Lionetti, Vincenzo</creator><creator>Recchia, Fabio A.</creator><creator>Czuriga, István</creator><creator>Édes, István</creator><creator>Papp, Zoltán</creator><general>Springer-Verlag</general><general>Springer Nature B.V</general><scope>C6C</scope><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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M7Z</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20120301</creationdate><title>Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure</title><author>Czuriga, Dániel ; 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2+
sensitivity of force production are dysregulated in a porcine model of pacing-induced heart failure (HF). The level of protein kinase A (PKA)-dependent cardiac troponin I (TnI) phosphorylation was lower in the myocardium surrounding the pacing electrode (pacing site) of the failing left ventricle (LV) than in the controls. Immunohistochemical assays of the LV pacing site pointed to isolated clusters of cardiomyocytes exhibiting a reduced level of phosphorylated TnI. Flow cytometry on isolated and permeabilized cardiomyocytes revealed a significantly larger cell-to-cell variation in the level of TnI phosphorylation of the LV pacing site than in the opposite region in HF or in either region in the controls: the interquartile range (IQR) on the distribution histogram of relative TnI phosphorylation was wider at the pacing site (IQR = 0.53) than that at the remote site of HF (IQR = 0.42;
P
= 0.0047) or that of the free wall of the control animals (IQR = 0.36;
P
= 0.0093). Additionally, the Ca
2+
sensitivities of isometric force production were higher and appeared to be more variable in single permeabilized cardiomyocytes from the HF pacing site than in the healthy myocardium. In conclusion, the level of PKA-dependent TnI phosphorylation and the Ca
2+
sensitivity of force production exhibited a high cell-to-cell variability at the LV pacing site, possibly explaining the abnormalities of the regional myocardial contractile function in a porcine model of pacing-induced HF.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer-Verlag</pub><pmid>22237651</pmid><doi>10.1007/s00395-012-0244-x</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Basic research in cardiology, 2012-03, Vol.107 (2), p.244-244, Article 244 |
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| language | eng |
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| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Blotting, Western Cardiac Pacing, Artificial Cardiology Cell Separation Disease Models, Animal Flow Cytometry Heart Failure - metabolism Immunohistochemistry Male Medicine Medicine & Public Health Myofibrils - metabolism Original Contribution Phosphorylation Swine Troponin I - metabolism |
| title | Cell-to-cell variability in troponin I phosphorylation in a porcine model of pacing-induced heart failure |
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