Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling
Calpain is activated following myocardial infarction and ablation of calpastatin (CAST), an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI). The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-inf...
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| Veröffentlicht in: | PloS one 2015-03, Vol.10 (3), p.e0120178-e0120178 |
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| creator | Ye, Tingqiao Wang, Qiang Zhang, Yan Song, Xiaofeng Yang, Dachun Li, De Li, Dan Su, Linan Yang, Yongjian Ma, Shuangtao |
| description | Calpain is activated following myocardial infarction and ablation of calpastatin (CAST), an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI). The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-infarction myocardial remodeling process.
We established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates.
The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.
Transgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling. |
| doi_str_mv | 10.1371/journal.pone.0120178 |
| format | Article |
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We established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates.
The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.
Transgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0120178</identifier><identifier>PMID: 25786109</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Ablation (Surgery) ; Activation ; Animals ; Attenuation ; Calpain ; Calpain - genetics ; Calpain - metabolism ; Calpastatin ; Cardiology ; Cardiomegaly - enzymology ; Cardiomegaly - genetics ; Cardiomegaly - mortality ; Cardiomegaly - pathology ; Cholesterol ; Collagen ; Collagen (type I) ; Collagen (type III) ; Collagen Type I - genetics ; Collagen Type I - metabolism ; Collagen Type III - genetics ; Collagen Type III - metabolism ; Comparative analysis ; Cytoskeletal Proteins - genetics ; Cytoskeletal Proteins - metabolism ; Diabetes ; Disease Models, Animal ; Enzyme Activation ; Female ; Fibrosis ; Gene Expression Regulation ; Genetic engineering ; Heart ; Heart attack ; Heart attacks ; Heart failure ; House mouse ; Humans ; Hypertrophy ; Hypotension ; Isoenzymes - genetics ; Isoenzymes - metabolism ; Laboratory animals ; Male ; Matrix Metalloproteinase Inhibitors - metabolism ; Matrix metalloproteinases ; Matrix Metalloproteinases, Secreted - genetics ; Matrix Metalloproteinases, Secreted - metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Myocardial infarction ; Myocardial Infarction - enzymology ; Myocardial Infarction - genetics ; Myocardial Infarction - mortality ; Myocardial Infarction - pathology ; Ostomy ; Overexpression ; Proteins ; Rodents ; Survival Analysis ; Transgenic animals ; Transgenic mice ; Ventricle ; Ventricular Function, Left - genetics ; Ventricular Remodeling - genetics</subject><ispartof>PloS one, 2015-03, Vol.10 (3), p.e0120178-e0120178</ispartof><rights>COPYRIGHT 2015 Public Library of Science</rights><rights>2015 Ye et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://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>2015 Ye et al 2015 Ye et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-884ba117236440f2dd14bd65f87a67395fc2fe9de9c4eaf1d39bf0f0c3dc0fa03</citedby><cites>FETCH-LOGICAL-c692t-884ba117236440f2dd14bd65f87a67395fc2fe9de9c4eaf1d39bf0f0c3dc0fa03</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/PMC4364764/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4364764/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23868,27926,27927,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25786109$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Peng, Tianqing</contributor><creatorcontrib>Ye, Tingqiao</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Song, Xiaofeng</creatorcontrib><creatorcontrib>Yang, Dachun</creatorcontrib><creatorcontrib>Li, De</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Su, Linan</creatorcontrib><creatorcontrib>Yang, Yongjian</creatorcontrib><creatorcontrib>Ma, Shuangtao</creatorcontrib><title>Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Calpain is activated following myocardial infarction and ablation of calpastatin (CAST), an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI). The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-infarction myocardial remodeling process.
We established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates.
The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.
Transgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling.</description><subject>Ablation (Surgery)</subject><subject>Activation</subject><subject>Animals</subject><subject>Attenuation</subject><subject>Calpain</subject><subject>Calpain - genetics</subject><subject>Calpain - metabolism</subject><subject>Calpastatin</subject><subject>Cardiology</subject><subject>Cardiomegaly - enzymology</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - mortality</subject><subject>Cardiomegaly - pathology</subject><subject>Cholesterol</subject><subject>Collagen</subject><subject>Collagen (type I)</subject><subject>Collagen (type III)</subject><subject>Collagen Type I - genetics</subject><subject>Collagen Type I - metabolism</subject><subject>Collagen Type III - genetics</subject><subject>Collagen Type III - metabolism</subject><subject>Comparative analysis</subject><subject>Cytoskeletal Proteins - genetics</subject><subject>Cytoskeletal Proteins - metabolism</subject><subject>Diabetes</subject><subject>Disease Models, Animal</subject><subject>Enzyme Activation</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Gene Expression Regulation</subject><subject>Genetic engineering</subject><subject>Heart</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>House mouse</subject><subject>Humans</subject><subject>Hypertrophy</subject><subject>Hypotension</subject><subject>Isoenzymes - genetics</subject><subject>Isoenzymes - metabolism</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Matrix Metalloproteinase Inhibitors - metabolism</subject><subject>Matrix metalloproteinases</subject><subject>Matrix Metalloproteinases, Secreted - genetics</subject><subject>Matrix Metalloproteinases, Secreted - metabolism</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - enzymology</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial Infarction - mortality</subject><subject>Myocardial Infarction - pathology</subject><subject>Ostomy</subject><subject>Overexpression</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Survival Analysis</subject><subject>Transgenic animals</subject><subject>Transgenic mice</subject><subject>Ventricle</subject><subject>Ventricular Function, Left - genetics</subject><subject>Ventricular Remodeling - genetics</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk0trGzEQx5fS0qRpv0FpDYXSHtaVVvvSpRBCH4aAoa-rGOthy2iljaQ1ybevbG-Ct-RQdJCY-c1_NCNNlr3GaI5Jgz9t3eAtmHnvrJwjXCDctE-yc0xJkdcFIk9PzmfZixC2CFWkrevn2VlRNW2NET3P3HInfS5vey9D0M7OnJpxMD2ECFHbmbYbvdIxHI3JADzqXXIlFKyYQYzSDhBlmPUuxFxbBZ4f3N2d4-CFBjPzsnNCGm3XL7NnCkyQr8b9Ivv99cuvq-_59fLb4uryOuc1LWLetuUKMG4KUpclUoUQuFyJulJtA3VDaKV4oSQVkvJSgsKC0JVCCnEiOFKAyEX29qjbGxfY2KvAcJ30KtognIjFkRAOtqz3ugN_xxxodjA4v2bgo-ZGssSTlAzRoqVlrTjQlrS4TFelXGFJk9bnMduw6qTg0kYPZiI69Vi9YWu3Y2Wqr6nLJPBhFPDuZpAhsk4HLo0BK91wuHeFcUrbJPTdP-jj1Y3UGlIB6VVcysv3ouyyLFIDcdHsuzR_hEpLyE7z9LGUTvZJwMdJQGKivI1rGEJgi58__p9d_pmy70_YjQQTN8GZYf-RwhQsjyD3LgQv1UOTMWL7ubjvBtvPBRvnIoW9OX2gh6D7QSB_AfcpCl8</recordid><startdate>20150318</startdate><enddate>20150318</enddate><creator>Ye, Tingqiao</creator><creator>Wang, Qiang</creator><creator>Zhang, Yan</creator><creator>Song, Xiaofeng</creator><creator>Yang, Dachun</creator><creator>Li, De</creator><creator>Li, Dan</creator><creator>Su, Linan</creator><creator>Yang, Yongjian</creator><creator>Ma, Shuangtao</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>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>20150318</creationdate><title>Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling</title><author>Ye, Tingqiao ; Wang, Qiang ; Zhang, Yan ; Song, Xiaofeng ; Yang, Dachun ; Li, De ; Li, Dan ; Su, Linan ; Yang, Yongjian ; Ma, Shuangtao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-884ba117236440f2dd14bd65f87a67395fc2fe9de9c4eaf1d39bf0f0c3dc0fa03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Ablation (Surgery)</topic><topic>Activation</topic><topic>Animals</topic><topic>Attenuation</topic><topic>Calpain</topic><topic>Calpain - genetics</topic><topic>Calpain - metabolism</topic><topic>Calpastatin</topic><topic>Cardiology</topic><topic>Cardiomegaly - enzymology</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - mortality</topic><topic>Cardiomegaly - pathology</topic><topic>Cholesterol</topic><topic>Collagen</topic><topic>Collagen (type I)</topic><topic>Collagen (type III)</topic><topic>Collagen Type I - genetics</topic><topic>Collagen Type I - metabolism</topic><topic>Collagen Type III - genetics</topic><topic>Collagen Type III - metabolism</topic><topic>Comparative analysis</topic><topic>Cytoskeletal Proteins - genetics</topic><topic>Cytoskeletal Proteins - metabolism</topic><topic>Diabetes</topic><topic>Disease Models, Animal</topic><topic>Enzyme Activation</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Gene Expression Regulation</topic><topic>Genetic engineering</topic><topic>Heart</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Heart failure</topic><topic>House mouse</topic><topic>Humans</topic><topic>Hypertrophy</topic><topic>Hypotension</topic><topic>Isoenzymes - genetics</topic><topic>Isoenzymes - metabolism</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Matrix Metalloproteinase Inhibitors - metabolism</topic><topic>Matrix metalloproteinases</topic><topic>Matrix Metalloproteinases, Secreted - genetics</topic><topic>Matrix Metalloproteinases, Secreted - metabolism</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Transgenic</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - enzymology</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial Infarction - mortality</topic><topic>Myocardial Infarction - pathology</topic><topic>Ostomy</topic><topic>Overexpression</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Survival Analysis</topic><topic>Transgenic animals</topic><topic>Transgenic mice</topic><topic>Ventricle</topic><topic>Ventricular Function, Left - genetics</topic><topic>Ventricular Remodeling - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ye, Tingqiao</creatorcontrib><creatorcontrib>Wang, Qiang</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><creatorcontrib>Song, Xiaofeng</creatorcontrib><creatorcontrib>Yang, Dachun</creatorcontrib><creatorcontrib>Li, De</creatorcontrib><creatorcontrib>Li, Dan</creatorcontrib><creatorcontrib>Su, Linan</creatorcontrib><creatorcontrib>Yang, Yongjian</creatorcontrib><creatorcontrib>Ma, Shuangtao</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 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>Ye, Tingqiao</au><au>Wang, Qiang</au><au>Zhang, Yan</au><au>Song, Xiaofeng</au><au>Yang, Dachun</au><au>Li, De</au><au>Li, Dan</au><au>Su, Linan</au><au>Yang, Yongjian</au><au>Ma, Shuangtao</au><au>Peng, Tianqing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2015-03-18</date><risdate>2015</risdate><volume>10</volume><issue>3</issue><spage>e0120178</spage><epage>e0120178</epage><pages>e0120178-e0120178</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Calpain is activated following myocardial infarction and ablation of calpastatin (CAST), an endogenous inhibitor of calpains, promotes left ventricular remodeling after myocardial infarction (MI). The present study aimed to investigate the effect of transgenic over-expression of CAST on the post-infarction myocardial remodeling process.
We established transgenic mice (TG) ubiquitously over-expressing human CAST protein and produced MI in TG mice and C57BL/6J wild-type (WT) littermates.
The CAST protein expression was profoundly upregulated in the myocardial tissue of TG mice compared with WT littermates (P < 0.01). Overexpression of CAST significantly reduced the infarct size (P < 0.01) and blunted MI-induced interventricular hypertrophy, global myocardial fibrosis and collagen I and collagen III deposition, hypotension and hemodynamic disturbances at 21 days after MI. Moreover, the MI-induced up-regulation and activation of calpains were obviously attenuated in CAST TG mice. MI-induced down-regulation of CAST was partially reversed in TG mice. Additionally, the MI-caused imbalance of matrix metalloproteinases and their inhibitors was improved in TG mice.
Transgenic over-expression of CAST inhibits calpain activation and attenuates post-infarction myocardial remodeling.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>25786109</pmid><doi>10.1371/journal.pone.0120178</doi><tpages>e0120178</tpages><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1664459701 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Ablation (Surgery) Activation Animals Attenuation Calpain Calpain - genetics Calpain - metabolism Calpastatin Cardiology Cardiomegaly - enzymology Cardiomegaly - genetics Cardiomegaly - mortality Cardiomegaly - pathology Cholesterol Collagen Collagen (type I) Collagen (type III) Collagen Type I - genetics Collagen Type I - metabolism Collagen Type III - genetics Collagen Type III - metabolism Comparative analysis Cytoskeletal Proteins - genetics Cytoskeletal Proteins - metabolism Diabetes Disease Models, Animal Enzyme Activation Female Fibrosis Gene Expression Regulation Genetic engineering Heart Heart attack Heart attacks Heart failure House mouse Humans Hypertrophy Hypotension Isoenzymes - genetics Isoenzymes - metabolism Laboratory animals Male Matrix Metalloproteinase Inhibitors - metabolism Matrix metalloproteinases Matrix Metalloproteinases, Secreted - genetics Matrix Metalloproteinases, Secreted - metabolism Mice Mice, Inbred C57BL Mice, Transgenic Myocardial infarction Myocardial Infarction - enzymology Myocardial Infarction - genetics Myocardial Infarction - mortality Myocardial Infarction - pathology Ostomy Overexpression Proteins Rodents Survival Analysis Transgenic animals Transgenic mice Ventricle Ventricular Function, Left - genetics Ventricular Remodeling - genetics |
| title | Over-expression of calpastatin inhibits calpain activation and attenuates post-infarction myocardial remodeling |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T10%3A14%3A29IST&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=Over-expression%20of%20calpastatin%20inhibits%20calpain%20activation%20and%20attenuates%20post-infarction%20myocardial%20remodeling&rft.jtitle=PloS%20one&rft.au=Ye,%20Tingqiao&rft.date=2015-03-18&rft.volume=10&rft.issue=3&rft.spage=e0120178&rft.epage=e0120178&rft.pages=e0120178-e0120178&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0120178&rft_dat=%3Cgale_plos_%3EA423951270%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=1664459701&rft_id=info:pmid/25786109&rft_galeid=A423951270&rft_doaj_id=oai_doaj_org_article_9703e9d0928946fca983814c699cf1e9&rfr_iscdi=true |