Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model

Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for αB-crystallin (αBC) and HSPB2, two s...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:American journal of physiology. Heart and circulatory physiology 2004-03, Vol.286 (3), p.H847-H855
Hauptverfasser: Morrison, Lisa E., Whittaker, Ross J., Klepper, Robert E., Wawrousek, Eric F., Glembotski, Christopher C.
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page H855
container_issue 3
container_start_page H847
container_title American journal of physiology. Heart and circulatory physiology
container_volume 286
creator Morrison, Lisa E.
Whittaker, Ross J.
Klepper, Robert E.
Wawrousek, Eric F.
Glembotski, Christopher C.
description Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for αB-crystallin (αBC) and HSPB2, two sHSPs that are expressed in high levels in the heart, are in close proximity to one another; as a result, both genes were disrupted in a recently generated knockout (KO) mouse line. The αBC/HSPB2 KO mouse line is currently the only model that features disruption of sHSPs normally expressed in the heart. Accordingly, we examined the cardiac morphology, function, and response to I/R-induced stress in αBC-HSPB2 KO mice. Initial gross, light microscopic and echocardiographic characterization showed that the morphological and functional properties of hearts from adult KO mice were indistinguishable from age-matched wild-type (WT) mice. Electron microscopy showed that, compared with WT mouse hearts, KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility; however, when compared with WT, after I/R, KO mouse hearts exhibited a twofold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, when compared with WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, whereas neither αBC nor HSPB2 is essential for myocardial development and function under nonstressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.
doi_str_mv 10.1152/ajpheart.00715.2003
format Article
fullrecord <record><control><sourceid>crossref</sourceid><recordid>TN_cdi_crossref_primary_10_1152_ajpheart_00715_2003</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>10_1152_ajpheart_00715_2003</sourcerecordid><originalsourceid>FETCH-LOGICAL-c247t-952435abca2125ccf36cc3f7a7194e865ad24f293d083e1dc70890dc4c0c3fd43</originalsourceid><addsrcrecordid>eNo1kEtOwzAURS0EEqWwAibegIs_cdIMaQUUgVTEZxw9nu3WVRJHdjKoxKbYCGsi5TO6urpXZ3AIuRR8JoSWV7DrthZiP-O8EHomOVdHZDIukgmtymMy4SpXLBdKn5KzlHacc13kakI-nkNtE3Uh0q_PBcO4Tz3UtW8ptIauXp4Wko6li6G32Pt2Q_utpc0-IETjh4a6GBrqE25t44FF29nohuRDy3xrBrSGGmhgYw8UoA9r2oQhjYRgbH1OThzUyV785ZS83d68LlfscX13v7x-ZCizomellpnS8I4ghdSITuWIyhVQiDKz81yDkZmTpTJ8rqwwWPB5yQ1myMebydSUqF8uxpBStK7qom8g7ivBq4PA6l9g9SOwOghU32vgaLA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model</title><source>American Physiological Society</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Morrison, Lisa E. ; Whittaker, Ross J. ; Klepper, Robert E. ; Wawrousek, Eric F. ; Glembotski, Christopher C.</creator><creatorcontrib>Morrison, Lisa E. ; Whittaker, Ross J. ; Klepper, Robert E. ; Wawrousek, Eric F. ; Glembotski, Christopher C.</creatorcontrib><description>Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for αB-crystallin (αBC) and HSPB2, two sHSPs that are expressed in high levels in the heart, are in close proximity to one another; as a result, both genes were disrupted in a recently generated knockout (KO) mouse line. The αBC/HSPB2 KO mouse line is currently the only model that features disruption of sHSPs normally expressed in the heart. Accordingly, we examined the cardiac morphology, function, and response to I/R-induced stress in αBC-HSPB2 KO mice. Initial gross, light microscopic and echocardiographic characterization showed that the morphological and functional properties of hearts from adult KO mice were indistinguishable from age-matched wild-type (WT) mice. Electron microscopy showed that, compared with WT mouse hearts, KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility; however, when compared with WT, after I/R, KO mouse hearts exhibited a twofold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, when compared with WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, whereas neither αBC nor HSPB2 is essential for myocardial development and function under nonstressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.</description><identifier>ISSN: 0363-6135</identifier><identifier>EISSN: 1522-1539</identifier><identifier>DOI: 10.1152/ajpheart.00715.2003</identifier><language>eng</language><ispartof>American journal of physiology. Heart and circulatory physiology, 2004-03, Vol.286 (3), p.H847-H855</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c247t-952435abca2125ccf36cc3f7a7194e865ad24f293d083e1dc70890dc4c0c3fd43</citedby><cites>FETCH-LOGICAL-c247t-952435abca2125ccf36cc3f7a7194e865ad24f293d083e1dc70890dc4c0c3fd43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids></links><search><creatorcontrib>Morrison, Lisa E.</creatorcontrib><creatorcontrib>Whittaker, Ross J.</creatorcontrib><creatorcontrib>Klepper, Robert E.</creatorcontrib><creatorcontrib>Wawrousek, Eric F.</creatorcontrib><creatorcontrib>Glembotski, Christopher C.</creatorcontrib><title>Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model</title><title>American journal of physiology. Heart and circulatory physiology</title><description>Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for αB-crystallin (αBC) and HSPB2, two sHSPs that are expressed in high levels in the heart, are in close proximity to one another; as a result, both genes were disrupted in a recently generated knockout (KO) mouse line. The αBC/HSPB2 KO mouse line is currently the only model that features disruption of sHSPs normally expressed in the heart. Accordingly, we examined the cardiac morphology, function, and response to I/R-induced stress in αBC-HSPB2 KO mice. Initial gross, light microscopic and echocardiographic characterization showed that the morphological and functional properties of hearts from adult KO mice were indistinguishable from age-matched wild-type (WT) mice. Electron microscopy showed that, compared with WT mouse hearts, KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility; however, when compared with WT, after I/R, KO mouse hearts exhibited a twofold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, when compared with WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, whereas neither αBC nor HSPB2 is essential for myocardial development and function under nonstressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.</description><issn>0363-6135</issn><issn>1522-1539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNo1kEtOwzAURS0EEqWwAibegIs_cdIMaQUUgVTEZxw9nu3WVRJHdjKoxKbYCGsi5TO6urpXZ3AIuRR8JoSWV7DrthZiP-O8EHomOVdHZDIukgmtymMy4SpXLBdKn5KzlHacc13kakI-nkNtE3Uh0q_PBcO4Tz3UtW8ptIauXp4Wko6li6G32Pt2Q_utpc0-IETjh4a6GBrqE25t44FF29nohuRDy3xrBrSGGmhgYw8UoA9r2oQhjYRgbH1OThzUyV785ZS83d68LlfscX13v7x-ZCizomellpnS8I4ghdSITuWIyhVQiDKz81yDkZmTpTJ8rqwwWPB5yQ1myMebydSUqF8uxpBStK7qom8g7ivBq4PA6l9g9SOwOghU32vgaLA</recordid><startdate>20040301</startdate><enddate>20040301</enddate><creator>Morrison, Lisa E.</creator><creator>Whittaker, Ross J.</creator><creator>Klepper, Robert E.</creator><creator>Wawrousek, Eric F.</creator><creator>Glembotski, Christopher C.</creator><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>20040301</creationdate><title>Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model</title><author>Morrison, Lisa E. ; Whittaker, Ross J. ; Klepper, Robert E. ; Wawrousek, Eric F. ; Glembotski, Christopher C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c247t-952435abca2125ccf36cc3f7a7194e865ad24f293d083e1dc70890dc4c0c3fd43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morrison, Lisa E.</creatorcontrib><creatorcontrib>Whittaker, Ross J.</creatorcontrib><creatorcontrib>Klepper, Robert E.</creatorcontrib><creatorcontrib>Wawrousek, Eric F.</creatorcontrib><creatorcontrib>Glembotski, Christopher C.</creatorcontrib><collection>CrossRef</collection><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morrison, Lisa E.</au><au>Whittaker, Ross J.</au><au>Klepper, Robert E.</au><au>Wawrousek, Eric F.</au><au>Glembotski, Christopher C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model</atitle><jtitle>American journal of physiology. Heart and circulatory physiology</jtitle><date>2004-03-01</date><risdate>2004</risdate><volume>286</volume><issue>3</issue><spage>H847</spage><epage>H855</epage><pages>H847-H855</pages><issn>0363-6135</issn><eissn>1522-1539</eissn><abstract>Overexpression studies have shown that the small heat shock proteins (sHSP) protect the myocardium from ischemia-reperfusion (I/R)-induced damage. However, gene deletion studies are necessary to demonstrate whether sHSPs are required for protection. The genes for αB-crystallin (αBC) and HSPB2, two sHSPs that are expressed in high levels in the heart, are in close proximity to one another; as a result, both genes were disrupted in a recently generated knockout (KO) mouse line. The αBC/HSPB2 KO mouse line is currently the only model that features disruption of sHSPs normally expressed in the heart. Accordingly, we examined the cardiac morphology, function, and response to I/R-induced stress in αBC-HSPB2 KO mice. Initial gross, light microscopic and echocardiographic characterization showed that the morphological and functional properties of hearts from adult KO mice were indistinguishable from age-matched wild-type (WT) mice. Electron microscopy showed that, compared with WT mouse hearts, KO mouse heart sarcomeres were relatively normal. Isolated perfused KO mouse hearts displayed normal contractility; however, when compared with WT, after I/R, KO mouse hearts exhibited a twofold reduction in contractile recovery, as well as increased necrosis and apoptosis. Additionally, when compared with WT, KO mouse hearts exhibited 43% less reduced glutathione, which is known to protect from I/R-induced damage. Thus, whereas neither αBC nor HSPB2 is essential for myocardial development and function under nonstressful conditions, one or both are required for maximal functional recovery and protection from I/R-induced necrosis and apoptosis.</abstract><doi>10.1152/ajpheart.00715.2003</doi></addata></record>
fulltext fulltext
identifier ISSN: 0363-6135
ispartof American journal of physiology. Heart and circulatory physiology, 2004-03, Vol.286 (3), p.H847-H855
issn 0363-6135
1522-1539
language eng
recordid cdi_crossref_primary_10_1152_ajpheart_00715_2003
source American Physiological Society; EZB-FREE-00999 freely available EZB journals
title Roles for αB-crystallin and HSPB2 in protecting the myocardium from ischemia-reperfusion-induced damage in a KO mouse model
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-26T00%3A15%3A21IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-crossref&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Roles%20for%20%CE%B1B-crystallin%20and%20HSPB2%20in%20protecting%20the%20myocardium%20from%20ischemia-reperfusion-induced%20damage%20in%20a%20KO%20mouse%20model&rft.jtitle=American%20journal%20of%20physiology.%20Heart%20and%20circulatory%20physiology&rft.au=Morrison,%20Lisa%20E.&rft.date=2004-03-01&rft.volume=286&rft.issue=3&rft.spage=H847&rft.epage=H855&rft.pages=H847-H855&rft.issn=0363-6135&rft.eissn=1522-1539&rft_id=info:doi/10.1152/ajpheart.00715.2003&rft_dat=%3Ccrossref%3E10_1152_ajpheart_00715_2003%3C/crossref%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/&rfr_iscdi=true