Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes
The objectives of this study were to analyse the effect of heart failure (HF) on several proteins of nuclear pore complex (NPC) and their relationship with the human ventricular function. A total of 88 human heart samples from ischemic (ICM, n = 52) and dilated (DCM, n = 36) patients undergoing hear...
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| creator | Tarazón, Estefanía Rivera, Miguel Roselló-Lletí, Esther Molina-Navarro, Maria Micaela Sánchez-Lázaro, Ignacio José España, Francisco Montero, José Anastasio Lago, Francisca González-Juanatey, José Ramón Portolés, Manuel |
| description | The objectives of this study were to analyse the effect of heart failure (HF) on several proteins of nuclear pore complex (NPC) and their relationship with the human ventricular function.
A total of 88 human heart samples from ischemic (ICM, n = 52) and dilated (DCM, n = 36) patients undergoing heart transplant and control donors (CNT, n = 9) were analyzed by Western blot. Subcellular distribution of nucleoporins was analysed by fluorescence and immunocytochemistry. When we compared protein levels according to etiology, ICM showed significant higher levels of NDC1 (65%, p |
| doi_str_mv | 10.1371/journal.pone.0048957 |
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A total of 88 human heart samples from ischemic (ICM, n = 52) and dilated (DCM, n = 36) patients undergoing heart transplant and control donors (CNT, n = 9) were analyzed by Western blot. Subcellular distribution of nucleoporins was analysed by fluorescence and immunocytochemistry. When we compared protein levels according to etiology, ICM showed significant higher levels of NDC1 (65%, p<0.0001), Nup160 (88%, p<0.0001) and Nup153 (137%, p = 0.004) than those of the CNT levels. Furthermore, DCM group showed significant differences for NDC1 (41%, p<0.0001), Nup160 (65%, p<0.0001), Nup153 (155%, p = 0.006) and Nup93 (88%, p<0.0001) compared with CNT. However, Nup155 and translocated promoter region (TPR) did not show significant differences in their levels in any etiology. Regarding the distribution of these proteins in cell nucleus, only NDC1 showed differences in HF. In addition, in the pathological group we obtained good relationship between the ventricular function parameters (LVEDD and LVESD) and Nup160 (r = -0382, p = 0.004; r = -0.290, p = 0.033; respectively).
This study shows alterations in specific proteins (NDC1, Nup160, Nup153 and Nup93) that compose NPC in ischaemic and dilated human heart. These changes, related to ventricular function, could be accompanied by alterations in the nucleocytoplasmic transport. Therefore, our findings may be the basis for a new approach to HF management.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0048957</identifier><identifier>PMID: 23152829</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Alcohol ; Biology ; Biomedical research ; Cardiology ; Cardiomyocytes ; Cardiomyopathy ; Ethics ; Etiology ; Female ; Fluorescence ; Heart ; Heart diseases ; Heart failure ; Heart Failure - etiology ; Heart Failure - metabolism ; Heart transplantation ; Heart Ventricles - metabolism ; Heart Ventricles - physiopathology ; Hospitals ; Humans ; Immunocytochemistry ; Ischemia ; Male ; Medicine ; Middle Aged ; Monoclonal antibodies ; Mutation ; Myocytes, Cardiac - metabolism ; Nuclear Pore Complex Proteins - metabolism ; Nuclear Proteins - metabolism ; Nuclei ; Nuclei (cytology) ; Nucleoporins ; Protein Transport ; Proteins ; Transplants & implants ; Values ; Ventricle</subject><ispartof>PloS one, 2012-11, Vol.7 (11), p.e48957-e48957</ispartof><rights>COPYRIGHT 2012 Public Library of Science</rights><rights>2012 Tarazón et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2012 Tarazón et al 2012 Tarazón et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-13993db1f41413e5d3930fb770eb4a31d0df495dc497c0691fa2e3602756104b3</citedby><cites>FETCH-LOGICAL-c692t-13993db1f41413e5d3930fb770eb4a31d0df495dc497c0691fa2e3602756104b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495918/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3495918/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23152829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tarazón, Estefanía</creatorcontrib><creatorcontrib>Rivera, Miguel</creatorcontrib><creatorcontrib>Roselló-Lletí, Esther</creatorcontrib><creatorcontrib>Molina-Navarro, Maria Micaela</creatorcontrib><creatorcontrib>Sánchez-Lázaro, Ignacio José</creatorcontrib><creatorcontrib>España, Francisco</creatorcontrib><creatorcontrib>Montero, José Anastasio</creatorcontrib><creatorcontrib>Lago, Francisca</creatorcontrib><creatorcontrib>González-Juanatey, José Ramón</creatorcontrib><creatorcontrib>Portolés, Manuel</creatorcontrib><title>Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>The objectives of this study were to analyse the effect of heart failure (HF) on several proteins of nuclear pore complex (NPC) and their relationship with the human ventricular function.
A total of 88 human heart samples from ischemic (ICM, n = 52) and dilated (DCM, n = 36) patients undergoing heart transplant and control donors (CNT, n = 9) were analyzed by Western blot. Subcellular distribution of nucleoporins was analysed by fluorescence and immunocytochemistry. When we compared protein levels according to etiology, ICM showed significant higher levels of NDC1 (65%, p<0.0001), Nup160 (88%, p<0.0001) and Nup153 (137%, p = 0.004) than those of the CNT levels. Furthermore, DCM group showed significant differences for NDC1 (41%, p<0.0001), Nup160 (65%, p<0.0001), Nup153 (155%, p = 0.006) and Nup93 (88%, p<0.0001) compared with CNT. However, Nup155 and translocated promoter region (TPR) did not show significant differences in their levels in any etiology. Regarding the distribution of these proteins in cell nucleus, only NDC1 showed differences in HF. In addition, in the pathological group we obtained good relationship between the ventricular function parameters (LVEDD and LVESD) and Nup160 (r = -0382, p = 0.004; r = -0.290, p = 0.033; respectively).
This study shows alterations in specific proteins (NDC1, Nup160, Nup153 and Nup93) that compose NPC in ischaemic and dilated human heart. These changes, related to ventricular function, could be accompanied by alterations in the nucleocytoplasmic transport. Therefore, our findings may be the basis for a new approach to HF management.</description><subject>Adult</subject><subject>Alcohol</subject><subject>Biology</subject><subject>Biomedical research</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiomyopathy</subject><subject>Ethics</subject><subject>Etiology</subject><subject>Female</subject><subject>Fluorescence</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart Failure - etiology</subject><subject>Heart Failure - metabolism</subject><subject>Heart transplantation</subject><subject>Heart Ventricles - metabolism</subject><subject>Heart Ventricles - physiopathology</subject><subject>Hospitals</subject><subject>Humans</subject><subject>Immunocytochemistry</subject><subject>Ischemia</subject><subject>Male</subject><subject>Medicine</subject><subject>Middle Aged</subject><subject>Monoclonal antibodies</subject><subject>Mutation</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Nuclear Pore Complex Proteins - metabolism</subject><subject>Nuclear Proteins - metabolism</subject><subject>Nuclei</subject><subject>Nuclei (cytology)</subject><subject>Nucleoporins</subject><subject>Protein Transport</subject><subject>Proteins</subject><subject>Transplants & implants</subject><subject>Values</subject><subject>Ventricle</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11rFDEUhgdRbK3-A9EBQfRi13zNZHIjlKJ2oVDwC7wKmXzMZskk22RGuv_erDstO9ILyUXCyXPe5LzJKYqXECwhpvDDJozRC7fcBq-XAJCGVfRRcQoZRosaAfz4aH1SPEtpA0CFm7p-WpwgDCvUIHZa_LrUIg6lEdaNUZfWq1HqVCbbeWusFH4o5Vr4LsesL_0oXebLbcisDP3W6dsymHI99sKXUkRlQ78Lcjfo9Lx4YoRL-sU0nxU_Pn_6fnG5uLr-sro4v1rImqFhATFjWLXQEEgg1pXCDAPTUgp0SwSGCihDWKUkYVSCmkEjkMY1QLSqISAtPiteH3S3LiQ-uZI4xLgCFUUNzsTqQKggNnwbbS_ijgdh-d9AiB3PHthcGq8rARAChja6Ji3VohGCqTwrAg2qm6z1cTptbHutpPZDFG4mOt_xds278JvjXASDe4F3k0AMN6NOA-9tkto54XUY870hhQ2tGN2jb_5BH65uojqRC7DehHyu3Ivyc5JtZJAAmqnlA1QeSvdW5i9kbI7PEt7PEjIz6NuhE2NKfPXt6_-z1z_n7Nsjdq2FG9YpuHGwwac5SA6gjCGlqM29yRDwfQfcucH3HcCnDshpr44f6D7p7svjP-FYAF8</recordid><startdate>20121112</startdate><enddate>20121112</enddate><creator>Tarazón, Estefanía</creator><creator>Rivera, Miguel</creator><creator>Roselló-Lletí, Esther</creator><creator>Molina-Navarro, Maria Micaela</creator><creator>Sánchez-Lázaro, Ignacio José</creator><creator>España, Francisco</creator><creator>Montero, José Anastasio</creator><creator>Lago, Francisca</creator><creator>González-Juanatey, José Ramón</creator><creator>Portolés, Manuel</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</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>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20121112</creationdate><title>Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes</title><author>Tarazón, Estefanía ; Rivera, Miguel ; Roselló-Lletí, Esther ; Molina-Navarro, Maria Micaela ; Sánchez-Lázaro, Ignacio José ; España, Francisco ; Montero, José Anastasio ; Lago, Francisca ; González-Juanatey, José Ramón ; Portolés, Manuel</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-13993db1f41413e5d3930fb770eb4a31d0df495dc497c0691fa2e3602756104b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adult</topic><topic>Alcohol</topic><topic>Biology</topic><topic>Biomedical research</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiomyopathy</topic><topic>Ethics</topic><topic>Etiology</topic><topic>Female</topic><topic>Fluorescence</topic><topic>Heart</topic><topic>Heart diseases</topic><topic>Heart failure</topic><topic>Heart Failure - etiology</topic><topic>Heart Failure - metabolism</topic><topic>Heart transplantation</topic><topic>Heart Ventricles - metabolism</topic><topic>Heart Ventricles - physiopathology</topic><topic>Hospitals</topic><topic>Humans</topic><topic>Immunocytochemistry</topic><topic>Ischemia</topic><topic>Male</topic><topic>Medicine</topic><topic>Middle Aged</topic><topic>Monoclonal antibodies</topic><topic>Mutation</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Nuclear Pore Complex Proteins - metabolism</topic><topic>Nuclear Proteins - metabolism</topic><topic>Nuclei</topic><topic>Nuclei (cytology)</topic><topic>Nucleoporins</topic><topic>Protein Transport</topic><topic>Proteins</topic><topic>Transplants & implants</topic><topic>Values</topic><topic>Ventricle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tarazón, Estefanía</creatorcontrib><creatorcontrib>Rivera, Miguel</creatorcontrib><creatorcontrib>Roselló-Lletí, Esther</creatorcontrib><creatorcontrib>Molina-Navarro, Maria Micaela</creatorcontrib><creatorcontrib>Sánchez-Lázaro, Ignacio José</creatorcontrib><creatorcontrib>España, Francisco</creatorcontrib><creatorcontrib>Montero, José Anastasio</creatorcontrib><creatorcontrib>Lago, Francisca</creatorcontrib><creatorcontrib>González-Juanatey, José Ramón</creatorcontrib><creatorcontrib>Portolés, Manuel</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</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 One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</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>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tarazón, Estefanía</au><au>Rivera, Miguel</au><au>Roselló-Lletí, Esther</au><au>Molina-Navarro, Maria Micaela</au><au>Sánchez-Lázaro, Ignacio José</au><au>España, Francisco</au><au>Montero, José Anastasio</au><au>Lago, Francisca</au><au>González-Juanatey, José Ramón</au><au>Portolés, Manuel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-11-12</date><risdate>2012</risdate><volume>7</volume><issue>11</issue><spage>e48957</spage><epage>e48957</epage><pages>e48957-e48957</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>The objectives of this study were to analyse the effect of heart failure (HF) on several proteins of nuclear pore complex (NPC) and their relationship with the human ventricular function.
A total of 88 human heart samples from ischemic (ICM, n = 52) and dilated (DCM, n = 36) patients undergoing heart transplant and control donors (CNT, n = 9) were analyzed by Western blot. Subcellular distribution of nucleoporins was analysed by fluorescence and immunocytochemistry. When we compared protein levels according to etiology, ICM showed significant higher levels of NDC1 (65%, p<0.0001), Nup160 (88%, p<0.0001) and Nup153 (137%, p = 0.004) than those of the CNT levels. Furthermore, DCM group showed significant differences for NDC1 (41%, p<0.0001), Nup160 (65%, p<0.0001), Nup153 (155%, p = 0.006) and Nup93 (88%, p<0.0001) compared with CNT. However, Nup155 and translocated promoter region (TPR) did not show significant differences in their levels in any etiology. Regarding the distribution of these proteins in cell nucleus, only NDC1 showed differences in HF. In addition, in the pathological group we obtained good relationship between the ventricular function parameters (LVEDD and LVESD) and Nup160 (r = -0382, p = 0.004; r = -0.290, p = 0.033; respectively).
This study shows alterations in specific proteins (NDC1, Nup160, Nup153 and Nup93) that compose NPC in ischaemic and dilated human heart. These changes, related to ventricular function, could be accompanied by alterations in the nucleocytoplasmic transport. Therefore, our findings may be the basis for a new approach to HF management.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23152829</pmid><doi>10.1371/journal.pone.0048957</doi><tpages>e48957</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
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| issn | 1932-6203 1932-6203 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Adult Alcohol Biology Biomedical research Cardiology Cardiomyocytes Cardiomyopathy Ethics Etiology Female Fluorescence Heart Heart diseases Heart failure Heart Failure - etiology Heart Failure - metabolism Heart transplantation Heart Ventricles - metabolism Heart Ventricles - physiopathology Hospitals Humans Immunocytochemistry Ischemia Male Medicine Middle Aged Monoclonal antibodies Mutation Myocytes, Cardiac - metabolism Nuclear Pore Complex Proteins - metabolism Nuclear Proteins - metabolism Nuclei Nuclei (cytology) Nucleoporins Protein Transport Proteins Transplants & implants Values Ventricle |
| title | Heart failure induces significant changes in nuclear pore complex of human cardiomyocytes |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-10T05%3A41%3A05IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Heart%20failure%20induces%20significant%20changes%20in%20nuclear%20pore%20complex%20of%20human%20cardiomyocytes&rft.jtitle=PloS%20one&rft.au=Taraz%C3%B3n,%20Estefan%C3%ADa&rft.date=2012-11-12&rft.volume=7&rft.issue=11&rft.spage=e48957&rft.epage=e48957&rft.pages=e48957-e48957&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0048957&rft_dat=%3Cgale_plos_%3EA477091407%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1335057283&rft_id=info:pmid/23152829&rft_galeid=A477091407&rft_doaj_id=oai_doaj_org_article_65a0220f78e64b7ea8aa9d7ead41f268&rfr_iscdi=true |