Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts
Abstract During development, epicardial cells act as progenitors for a large fraction of non-myocyte cardiac cells. Expression and function of molecules of the desmosome in the postnatal epicardium has not been studied. The objective of this study was to assess the expression of desmosomal molecules...
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| Veröffentlicht in: | Cell communication & adhesion 2011-08, Vol.18 (4), p.73-84 |
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| creator | Matthes, Stephanie A. Taffet, Steven Delmar, Mario |
| description | Abstract
During development, epicardial cells act as progenitors for a large fraction of non-myocyte cardiac cells. Expression and function of molecules of the desmosome in the postnatal epicardium has not been studied. The objective of this study was to assess the expression of desmosomal molecules, and the functional importance of the desmosomal protein plakophilin-2 (PKP2), in epicardial and epicardium-derived cells. Epicardial explants were obtained from neonatal rat hearts. Presence of mechanical junction proteins was assessed by immunocytochemistry. Explants after PKP2 knockdown showed increased abundance of alpha smooth muscle actin-positive cells, increased abundance of lipid markers, enhanced cell migration velocity and increased abundance of a marker of cell proliferation. We conclude that a population of non-excitable, cardiac-resident cells express desmosomal molecules and, in vitro, show functional properties (including lipid accumulation) that depend on PKP2 expression. The possible relevance of our data to the pathophysiology of arrhythmogenic right ventricular cardiomyopathy, is discussed. |
| doi_str_mv | 10.3109/15419061.2011.621561 |
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During development, epicardial cells act as progenitors for a large fraction of non-myocyte cardiac cells. Expression and function of molecules of the desmosome in the postnatal epicardium has not been studied. The objective of this study was to assess the expression of desmosomal molecules, and the functional importance of the desmosomal protein plakophilin-2 (PKP2), in epicardial and epicardium-derived cells. Epicardial explants were obtained from neonatal rat hearts. Presence of mechanical junction proteins was assessed by immunocytochemistry. Explants after PKP2 knockdown showed increased abundance of alpha smooth muscle actin-positive cells, increased abundance of lipid markers, enhanced cell migration velocity and increased abundance of a marker of cell proliferation. We conclude that a population of non-excitable, cardiac-resident cells express desmosomal molecules and, in vitro, show functional properties (including lipid accumulation) that depend on PKP2 expression. The possible relevance of our data to the pathophysiology of arrhythmogenic right ventricular cardiomyopathy, is discussed.</description><identifier>ISSN: 1541-9061</identifier><identifier>EISSN: 1543-5180</identifier><identifier>DOI: 10.3109/15419061.2011.621561</identifier><identifier>PMID: 21985446</identifier><language>eng</language><publisher>England: Informa Healthcare</publisher><subject>Actins - metabolism ; Animals ; Animals, Newborn ; arrhythmogenic ; arrhythmogenic cardiomyopathy (AC) ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; desmosome ; Desmosomes - metabolism ; epicardial cells ; Epicardium ; Pericardium - cytology ; plakophilin-2 ; Plakophilins - antagonists & inhibitors ; Plakophilins - metabolism ; Rats ; rightventricular cardiomyopathy (ARVC) ; RNA Interference ; RNA, Small Interfering</subject><ispartof>Cell communication & adhesion, 2011-08, Vol.18 (4), p.73-84</ispartof><rights>2011 Informa Healthcare USA, Inc. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c518t-bcfc2b2b0d92e0873611c11948f07dd1425ca0e412b9486faed853aab1aa46263</citedby><cites>FETCH-LOGICAL-c518t-bcfc2b2b0d92e0873611c11948f07dd1425ca0e412b9486faed853aab1aa46263</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.tandfonline.com/doi/pdf/10.3109/15419061.2011.621561$$EPDF$$P50$$Ginformahealthcare$$H</linktopdf><linktohtml>$$Uhttps://www.tandfonline.com/doi/full/10.3109/15419061.2011.621561$$EHTML$$P50$$Ginformahealthcare$$H</linktohtml><link.rule.ids>230,314,780,784,885,27502,27924,27925,59143,59144,61218,61219</link.rule.ids><linktorsrc>$$Uhttps://www.tandfonline.com/doi/abs/10.3109/15419061.2011.621561$$EView_record_in_Taylor_&_Francis$$FView_record_in_$$GTaylor_&_Francis</linktorsrc><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21985446$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Matthes, Stephanie A.</creatorcontrib><creatorcontrib>Taffet, Steven</creatorcontrib><creatorcontrib>Delmar, Mario</creatorcontrib><title>Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts</title><title>Cell communication & adhesion</title><addtitle>Cell Commun Adhes</addtitle><description>Abstract
During development, epicardial cells act as progenitors for a large fraction of non-myocyte cardiac cells. Expression and function of molecules of the desmosome in the postnatal epicardium has not been studied. The objective of this study was to assess the expression of desmosomal molecules, and the functional importance of the desmosomal protein plakophilin-2 (PKP2), in epicardial and epicardium-derived cells. Epicardial explants were obtained from neonatal rat hearts. Presence of mechanical junction proteins was assessed by immunocytochemistry. Explants after PKP2 knockdown showed increased abundance of alpha smooth muscle actin-positive cells, increased abundance of lipid markers, enhanced cell migration velocity and increased abundance of a marker of cell proliferation. We conclude that a population of non-excitable, cardiac-resident cells express desmosomal molecules and, in vitro, show functional properties (including lipid accumulation) that depend on PKP2 expression. The possible relevance of our data to the pathophysiology of arrhythmogenic right ventricular cardiomyopathy, is discussed.</description><subject>Actins - metabolism</subject><subject>Animals</subject><subject>Animals, Newborn</subject><subject>arrhythmogenic</subject><subject>arrhythmogenic cardiomyopathy (AC)</subject><subject>Cell Differentiation</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>desmosome</subject><subject>Desmosomes - metabolism</subject><subject>epicardial cells</subject><subject>Epicardium</subject><subject>Pericardium - cytology</subject><subject>plakophilin-2</subject><subject>Plakophilins - antagonists & inhibitors</subject><subject>Plakophilins - metabolism</subject><subject>Rats</subject><subject>rightventricular cardiomyopathy (ARVC)</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering</subject><issn>1541-9061</issn><issn>1543-5180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1TAQhSMEoqXwBgh5x4ZcPI6Tm2yKqgpopUp0UdbWxD-Ni2Nf7KSoK14d56at6KYrW-MzZ-b4K4r3QDcV0O4z1Bw62sCGUYBNw6Bu4EVxmMtVWUNLX-7vUC6ag-JNSjeUMkZ5_bo4YNC1NefNYfH30uGvsBuss75kBL0i06DJaK8jTjb4T0RZY3TUfrL7wiqJ6JMJcVxLwRCpnUtE6WhvtSImhnHvo3dWYlR2HheR18HjhI5kbzJojFN6W7wy6JJ-d38eFT-_fb06PSsvfnw_Pz25KGXOMpW9NJL1rKeqY5q226oBkAAdbw3dKgWc1RKp5sD6XGsMatXWFWIPiLxhTXVUHK--u7kftZI5T0QndtGOGO9EQCuevng7iOtwKyqWx7FtNvh4bxDD71mnSYw2Lakxp5qT6CirWNsyyEq-KmUMKUVtHqcAFQs68YBOLOjEii63ffh_w8emB1ZZ8GUVWL__-j8hOiUmvHMhmgxE2rTYPzvi-IlDRuCmIQPS4ibM0WcAz-_4DzlAvu0</recordid><startdate>201108</startdate><enddate>201108</enddate><creator>Matthes, Stephanie A.</creator><creator>Taffet, Steven</creator><creator>Delmar, Mario</creator><general>Informa Healthcare</general><general>Taylor & Francis</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>5PM</scope></search><sort><creationdate>201108</creationdate><title>Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts</title><author>Matthes, Stephanie A. ; Taffet, Steven ; Delmar, Mario</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c518t-bcfc2b2b0d92e0873611c11948f07dd1425ca0e412b9486faed853aab1aa46263</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Actins - metabolism</topic><topic>Animals</topic><topic>Animals, Newborn</topic><topic>arrhythmogenic</topic><topic>arrhythmogenic cardiomyopathy (AC)</topic><topic>Cell Differentiation</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>desmosome</topic><topic>Desmosomes - metabolism</topic><topic>epicardial cells</topic><topic>Epicardium</topic><topic>Pericardium - cytology</topic><topic>plakophilin-2</topic><topic>Plakophilins - antagonists & inhibitors</topic><topic>Plakophilins - metabolism</topic><topic>Rats</topic><topic>rightventricular cardiomyopathy (ARVC)</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Matthes, Stephanie A.</creatorcontrib><creatorcontrib>Taffet, Steven</creatorcontrib><creatorcontrib>Delmar, Mario</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>PubMed Central (Full Participant titles)</collection><jtitle>Cell communication & adhesion</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext_linktorsrc</fulltext></delivery><addata><au>Matthes, Stephanie A.</au><au>Taffet, Steven</au><au>Delmar, Mario</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts</atitle><jtitle>Cell communication & adhesion</jtitle><addtitle>Cell Commun Adhes</addtitle><date>2011-08</date><risdate>2011</risdate><volume>18</volume><issue>4</issue><spage>73</spage><epage>84</epage><pages>73-84</pages><issn>1541-9061</issn><eissn>1543-5180</eissn><abstract>Abstract
During development, epicardial cells act as progenitors for a large fraction of non-myocyte cardiac cells. Expression and function of molecules of the desmosome in the postnatal epicardium has not been studied. The objective of this study was to assess the expression of desmosomal molecules, and the functional importance of the desmosomal protein plakophilin-2 (PKP2), in epicardial and epicardium-derived cells. Epicardial explants were obtained from neonatal rat hearts. Presence of mechanical junction proteins was assessed by immunocytochemistry. Explants after PKP2 knockdown showed increased abundance of alpha smooth muscle actin-positive cells, increased abundance of lipid markers, enhanced cell migration velocity and increased abundance of a marker of cell proliferation. We conclude that a population of non-excitable, cardiac-resident cells express desmosomal molecules and, in vitro, show functional properties (including lipid accumulation) that depend on PKP2 expression. The possible relevance of our data to the pathophysiology of arrhythmogenic right ventricular cardiomyopathy, is discussed.</abstract><cop>England</cop><pub>Informa Healthcare</pub><pmid>21985446</pmid><doi>10.3109/15419061.2011.621561</doi><tpages>12</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Actins - metabolism Animals Animals, Newborn arrhythmogenic arrhythmogenic cardiomyopathy (AC) Cell Differentiation Cell Movement Cell Proliferation Cells, Cultured desmosome Desmosomes - metabolism epicardial cells Epicardium Pericardium - cytology plakophilin-2 Plakophilins - antagonists & inhibitors Plakophilins - metabolism Rats rightventricular cardiomyopathy (ARVC) RNA Interference RNA, Small Interfering |
| title | Plakophilin-2 and the migration, differentiation and transformation of cells derived from the epicardium of neonatal rat hearts |
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