Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion
Myocardial infarction animal studies are used to study disease mechanisms and new treatment options. Typically, myocardial infarction (MI) is induced by permanent occlusion of the left anterior descending artery. Since in MI patients coronary blood flow is often restored new experimental models bett...
Gespeichert in:
Veröffentlicht in: | SpringerPlus 2015-07, Vol.4 (1), p.336-336, Article 336 |
---|---|
Hauptverfasser: | , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 336 |
---|---|
container_issue | 1 |
container_start_page | 336 |
container_title | SpringerPlus |
container_volume | 4 |
creator | van Zuylen, Vanessa-Leigh den Haan, Melina C Roelofs, Helene Fibbe, Willem E Schalij, Martin J Atsma, Douwe E |
description | Myocardial infarction animal studies are used to study disease mechanisms and new treatment options. Typically, myocardial infarction (MI) is induced by permanent occlusion of the left anterior descending artery. Since in MI patients coronary blood flow is often restored new experimental models better reflecting clinical practice are needed. Here, permanent ischemia MI (PI group) was compared with transient ischemia (45 min) (IR group) in immunodeficient NOD/
Scid
mice. Cardiac function, infarct size, wall thickness and total collagen deposition were significantly reduced only in PI mice. Cardiac inflammatory cells and serum cytokine levels were less dynamic in IR animals compared to PI. So although IR better reflects clinical practice, it is secondary to PI for investigating cell therapy, since it induces too little damage to provide a measurable therapeutic window. MI did result in significant changes in the inflammatory state, indicating this immunodeficient mouse strain is valuable to study human cell therapy. |
doi_str_mv | 10.1186/s40064-015-1128-y |
format | Article |
fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4498004</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1868326651</sourcerecordid><originalsourceid>FETCH-LOGICAL-c503t-62cd928867d0f4f1099a6670a53ffb420082358b4eaee5886df6add6ba9cbe523</originalsourceid><addsrcrecordid>eNqFks1u1DAQxyNERau2D8AFWeLCJdR2HMfhgIRaPioVegDOlmOPu66SeLGTSrnxDrwhT8Is264WJIQvHnl-8_d8FcVTRl8ypuRZFpRKUVJWl4xxVS6PiiPO2qpkirLHe_ZhcZrzLcUjGyYa-qQ45JKpuqnUUTF_XKI1yQXTkzB6k-wU4kiG6KDP-EI-XV-cfbbBkSFYID4mYqHvybSCZNYLSZABg1avyBrSYEYYJxKyXcEQDLnLO_vn9x8JEPFzRv2T4sCbPsPp_X1cfH339sv5h_Lq-v3l-Zur0ta0mkrJrWu5UrJx1AvPaNsaKRtq6sr7TnBKFa9q1QkwADVyzkvjnOxMazuoeXVcvN7qruduAGcxu2R6vU5hMGnR0QT9p2cMK30T77QQraJUoMCLe4EUv82QJz1gRdgArDTOWeMgVMWlrNn_Udk2nDP-O63nf6G3cU4jdmIjKFnFuJBIsS1lU8w5gd_lzajerIDeroDGFdCbFdALxjzbL3gX8TBwBPgWyOgabyDtff1P1V8csr8Q</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1866131246</pqid></control><display><type>article</type><title>Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion</title><source>SpringerOpen</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>EZB Electronic Journals Library</source><source>PubMed Central Open Access</source><creator>van Zuylen, Vanessa-Leigh ; den Haan, Melina C ; Roelofs, Helene ; Fibbe, Willem E ; Schalij, Martin J ; Atsma, Douwe E</creator><creatorcontrib>van Zuylen, Vanessa-Leigh ; den Haan, Melina C ; Roelofs, Helene ; Fibbe, Willem E ; Schalij, Martin J ; Atsma, Douwe E</creatorcontrib><description>Myocardial infarction animal studies are used to study disease mechanisms and new treatment options. Typically, myocardial infarction (MI) is induced by permanent occlusion of the left anterior descending artery. Since in MI patients coronary blood flow is often restored new experimental models better reflecting clinical practice are needed. Here, permanent ischemia MI (PI group) was compared with transient ischemia (45 min) (IR group) in immunodeficient NOD/
Scid
mice. Cardiac function, infarct size, wall thickness and total collagen deposition were significantly reduced only in PI mice. Cardiac inflammatory cells and serum cytokine levels were less dynamic in IR animals compared to PI. So although IR better reflects clinical practice, it is secondary to PI for investigating cell therapy, since it induces too little damage to provide a measurable therapeutic window. MI did result in significant changes in the inflammatory state, indicating this immunodeficient mouse strain is valuable to study human cell therapy.</description><identifier>ISSN: 2193-1801</identifier><identifier>EISSN: 2193-1801</identifier><identifier>DOI: 10.1186/s40064-015-1128-y</identifier><identifier>PMID: 26185738</identifier><language>eng</language><publisher>Cham: Springer International Publishing</publisher><subject>Humanities and Social Sciences ; Medicine ; multidisciplinary ; Science ; Science (multidisciplinary)</subject><ispartof>SpringerPlus, 2015-07, Vol.4 (1), p.336-336, Article 336</ispartof><rights>van Zuylen et al. 2015</rights><rights>SpringerPlus is a copyright of Springer, 2015.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-62cd928867d0f4f1099a6670a53ffb420082358b4eaee5886df6add6ba9cbe523</citedby><cites>FETCH-LOGICAL-c503t-62cd928867d0f4f1099a6670a53ffb420082358b4eaee5886df6add6ba9cbe523</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/PMC4498004/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4498004/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27926,27927,41122,42191,51578,53793,53795</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26185738$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>van Zuylen, Vanessa-Leigh</creatorcontrib><creatorcontrib>den Haan, Melina C</creatorcontrib><creatorcontrib>Roelofs, Helene</creatorcontrib><creatorcontrib>Fibbe, Willem E</creatorcontrib><creatorcontrib>Schalij, Martin J</creatorcontrib><creatorcontrib>Atsma, Douwe E</creatorcontrib><title>Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion</title><title>SpringerPlus</title><addtitle>SpringerPlus</addtitle><addtitle>Springerplus</addtitle><description>Myocardial infarction animal studies are used to study disease mechanisms and new treatment options. Typically, myocardial infarction (MI) is induced by permanent occlusion of the left anterior descending artery. Since in MI patients coronary blood flow is often restored new experimental models better reflecting clinical practice are needed. Here, permanent ischemia MI (PI group) was compared with transient ischemia (45 min) (IR group) in immunodeficient NOD/
Scid
mice. Cardiac function, infarct size, wall thickness and total collagen deposition were significantly reduced only in PI mice. Cardiac inflammatory cells and serum cytokine levels were less dynamic in IR animals compared to PI. So although IR better reflects clinical practice, it is secondary to PI for investigating cell therapy, since it induces too little damage to provide a measurable therapeutic window. MI did result in significant changes in the inflammatory state, indicating this immunodeficient mouse strain is valuable to study human cell therapy.</description><subject>Humanities and Social Sciences</subject><subject>Medicine</subject><subject>multidisciplinary</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><issn>2193-1801</issn><issn>2193-1801</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFks1u1DAQxyNERau2D8AFWeLCJdR2HMfhgIRaPioVegDOlmOPu66SeLGTSrnxDrwhT8Is264WJIQvHnl-8_d8FcVTRl8ypuRZFpRKUVJWl4xxVS6PiiPO2qpkirLHe_ZhcZrzLcUjGyYa-qQ45JKpuqnUUTF_XKI1yQXTkzB6k-wU4kiG6KDP-EI-XV-cfbbBkSFYID4mYqHvybSCZNYLSZABg1avyBrSYEYYJxKyXcEQDLnLO_vn9x8JEPFzRv2T4sCbPsPp_X1cfH339sv5h_Lq-v3l-Zur0ta0mkrJrWu5UrJx1AvPaNsaKRtq6sr7TnBKFa9q1QkwADVyzkvjnOxMazuoeXVcvN7qruduAGcxu2R6vU5hMGnR0QT9p2cMK30T77QQraJUoMCLe4EUv82QJz1gRdgArDTOWeMgVMWlrNn_Udk2nDP-O63nf6G3cU4jdmIjKFnFuJBIsS1lU8w5gd_lzajerIDeroDGFdCbFdALxjzbL3gX8TBwBPgWyOgabyDtff1P1V8csr8Q</recordid><startdate>20150710</startdate><enddate>20150710</enddate><creator>van Zuylen, Vanessa-Leigh</creator><creator>den Haan, Melina C</creator><creator>Roelofs, Helene</creator><creator>Fibbe, Willem E</creator><creator>Schalij, Martin J</creator><creator>Atsma, Douwe E</creator><general>Springer International Publishing</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X2</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FK</scope><scope>ABJCF</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>BKSAR</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>JQ2</scope><scope>K7-</scope><scope>KB.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M7P</scope><scope>M7S</scope><scope>P5Z</scope><scope>P62</scope><scope>PATMY</scope><scope>PCBAR</scope><scope>PDBOC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>7X8</scope><scope>7QO</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope><scope>5PM</scope></search><sort><creationdate>20150710</creationdate><title>Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion</title><author>van Zuylen, Vanessa-Leigh ; den Haan, Melina C ; Roelofs, Helene ; Fibbe, Willem E ; Schalij, Martin J ; Atsma, Douwe E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-62cd928867d0f4f1099a6670a53ffb420082358b4eaee5886df6add6ba9cbe523</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Humanities and Social Sciences</topic><topic>Medicine</topic><topic>multidisciplinary</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van Zuylen, Vanessa-Leigh</creatorcontrib><creatorcontrib>den Haan, Melina C</creatorcontrib><creatorcontrib>Roelofs, Helene</creatorcontrib><creatorcontrib>Fibbe, Willem E</creatorcontrib><creatorcontrib>Schalij, Martin J</creatorcontrib><creatorcontrib>Atsma, Douwe E</creatorcontrib><collection>SpringerOpen</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Agricultural Science Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Database (1962 - current)</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>ProQuest Natural Science Collection</collection><collection>Earth, Atmospheric & Aquatic Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Computer Science Collection</collection><collection>Computer science database</collection><collection>https://resources.nclive.org/materials</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Environmental Science Database</collection><collection>Earth, Atmospheric & Aquatic Science Database</collection><collection>Materials science collection</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering collection</collection><collection>Environmental Science Collection</collection><collection>MEDLINE - Academic</collection><collection>Biotechnology Research Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>SpringerPlus</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van Zuylen, Vanessa-Leigh</au><au>den Haan, Melina C</au><au>Roelofs, Helene</au><au>Fibbe, Willem E</au><au>Schalij, Martin J</au><au>Atsma, Douwe E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion</atitle><jtitle>SpringerPlus</jtitle><stitle>SpringerPlus</stitle><addtitle>Springerplus</addtitle><date>2015-07-10</date><risdate>2015</risdate><volume>4</volume><issue>1</issue><spage>336</spage><epage>336</epage><pages>336-336</pages><artnum>336</artnum><issn>2193-1801</issn><eissn>2193-1801</eissn><abstract>Myocardial infarction animal studies are used to study disease mechanisms and new treatment options. Typically, myocardial infarction (MI) is induced by permanent occlusion of the left anterior descending artery. Since in MI patients coronary blood flow is often restored new experimental models better reflecting clinical practice are needed. Here, permanent ischemia MI (PI group) was compared with transient ischemia (45 min) (IR group) in immunodeficient NOD/
Scid
mice. Cardiac function, infarct size, wall thickness and total collagen deposition were significantly reduced only in PI mice. Cardiac inflammatory cells and serum cytokine levels were less dynamic in IR animals compared to PI. So although IR better reflects clinical practice, it is secondary to PI for investigating cell therapy, since it induces too little damage to provide a measurable therapeutic window. MI did result in significant changes in the inflammatory state, indicating this immunodeficient mouse strain is valuable to study human cell therapy.</abstract><cop>Cham</cop><pub>Springer International Publishing</pub><pmid>26185738</pmid><doi>10.1186/s40064-015-1128-y</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 2193-1801 |
ispartof | SpringerPlus, 2015-07, Vol.4 (1), p.336-336, Article 336 |
issn | 2193-1801 2193-1801 |
language | eng |
recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_4498004 |
source | SpringerOpen; PubMed Central; Free Full-Text Journals in Chemistry; EZB Electronic Journals Library; PubMed Central Open Access |
subjects | Humanities and Social Sciences Medicine multidisciplinary Science Science (multidisciplinary) |
title | Myocardial infarction models in NOD/Scid mice for cell therapy research: permanent ischemia vs ischemia–reperfusion |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-17T16%3A58%3A28IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Myocardial%20infarction%20models%20in%20NOD/Scid%20mice%20for%20cell%20therapy%20research:%20permanent%20ischemia%20vs%20ischemia%E2%80%93reperfusion&rft.jtitle=SpringerPlus&rft.au=van%20Zuylen,%20Vanessa-Leigh&rft.date=2015-07-10&rft.volume=4&rft.issue=1&rft.spage=336&rft.epage=336&rft.pages=336-336&rft.artnum=336&rft.issn=2193-1801&rft.eissn=2193-1801&rft_id=info:doi/10.1186/s40064-015-1128-y&rft_dat=%3Cproquest_pubme%3E1868326651%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1866131246&rft_id=info:pmid/26185738&rfr_iscdi=true |