Locally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction
Identifieur interne : 001E63 ( Pmc/Checkpoint ); précédent : 001E62; suivant : 001E64Locally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction
Auteurs : Melissa Touvron [France] ; Brigitte Escoubet [France] ; Mathias Mericskay [France] ; Aude Angelini [France] ; Luciane Lamotte [France] ; Maria Paola Santini [Royaume-Uni] ; Nadia Rosenthal [Royaume-Uni, Italie, Australie] ; Dominique Daegelen [France] ; David Tuil [France] ; Jean-François Decaux [France]Source :
- Disease Models & Mechanisms [ 1754-8403 ] ; 2012.
Abstract
Cardiac fibrosis is critically involved in the adverse remodeling accompanying dilated cardiomyopathies (DCMs), which leads to cardiac dysfunction and heart failure (HF). Connective tissue growth factor (CTGF), a profibrotic cytokine, plays a key role in this deleterious process. Some beneficial effects of IGF1 on cardiomyopathy have been described, but its potential role in improving DCM is less well characterized. We investigated the consequences of expressing a cardiac-specific transgene encoding locally acting IGF1 propeptide (muscle-produced IGF1; mIGF1) on disease progression in a mouse model of DCM [cardiac-specific and inducible serum response factor (
Url:
DOI: 10.1242/dmm.009456
PubMed: 22563064
PubMed Central: 3380711
Affiliations:
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<affiliation wicri:level="1"><nlm:aff id="af11-0050481">Australian Regenerative Medicine Institute/EMBL Australia, Monash University, Melbourne, VIC 3800, Australia</nlm:aff>
<country xml:lang="fr">Australie</country>
<wicri:regionArea>Australian Regenerative Medicine Institute/EMBL Australia, Monash University, Melbourne, VIC 3800</wicri:regionArea>
<wicri:noRegion>VIC 3800</wicri:noRegion>
</affiliation>
</author>
<author><name sortKey="Daegelen, Dominique" sort="Daegelen, Dominique" uniqKey="Daegelen D" first="Dominique" last="Daegelen">Dominique Daegelen</name>
<affiliation wicri:level="1"><nlm:aff id="af1-0050481">INSERM, U1016, Institut Cochin, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM, U1016, Institut Cochin, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af2-0050481">CNRS, UMR8104, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CNRS, UMR8104, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="4"><nlm:aff id="af3-0050481">Université Paris Descartes, F-75006 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Descartes, F-75006 Paris</wicri:regionArea>
<wicri:noRegion>75006 Paris</wicri:noRegion>
<orgName type="university">Université Paris-Descartes</orgName>
<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Tuil, David" sort="Tuil, David" uniqKey="Tuil D" first="David" last="Tuil">David Tuil</name>
<affiliation wicri:level="1"><nlm:aff id="af1-0050481">INSERM, U1016, Institut Cochin, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM, U1016, Institut Cochin, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af2-0050481">CNRS, UMR8104, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CNRS, UMR8104, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="4"><nlm:aff id="af3-0050481">Université Paris Descartes, F-75006 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Descartes, F-75006 Paris</wicri:regionArea>
<wicri:noRegion>75006 Paris</wicri:noRegion>
<orgName type="university">Université Paris-Descartes</orgName>
<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
</affiliation>
</author>
<author><name sortKey="Decaux, Jean Francois" sort="Decaux, Jean Francois" uniqKey="Decaux J" first="Jean-François" last="Decaux">Jean-François Decaux</name>
<affiliation wicri:level="1"><nlm:aff id="af1-0050481">INSERM, U1016, Institut Cochin, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>INSERM, U1016, Institut Cochin, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="1"><nlm:aff id="af2-0050481">CNRS, UMR8104, F-75014 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>CNRS, UMR8104, F-75014 Paris</wicri:regionArea>
<wicri:noRegion>75014 Paris</wicri:noRegion>
<wicri:noRegion>75014 Paris</wicri:noRegion>
</affiliation>
<affiliation wicri:level="4"><nlm:aff id="af3-0050481">Université Paris Descartes, F-75006 Paris, France</nlm:aff>
<country xml:lang="fr">France</country>
<wicri:regionArea>Université Paris Descartes, F-75006 Paris</wicri:regionArea>
<wicri:noRegion>75006 Paris</wicri:noRegion>
<orgName type="university">Université Paris-Descartes</orgName>
<placeName><settlement type="city">Paris</settlement>
<region type="region" nuts="2">Île-de-France</region>
</placeName>
</affiliation>
</author>
</analytic>
<series><title level="j">Disease Models & Mechanisms</title>
<idno type="ISSN">1754-8403</idno>
<idno type="eISSN">1754-8411</idno>
<imprint><date when="2012">2012</date>
</imprint>
</series>
</biblStruct>
</sourceDesc>
</fileDesc>
<profileDesc><textClass></textClass>
</profileDesc>
</teiHeader>
<front><div type="abstract" xml:lang="en"><title>SUMMARY</title>
<p>Cardiac fibrosis is critically involved in the adverse remodeling accompanying dilated cardiomyopathies (DCMs), which leads to cardiac dysfunction and heart failure (HF). Connective tissue growth factor (CTGF), a profibrotic cytokine, plays a key role in this deleterious process. Some beneficial effects of IGF1 on cardiomyopathy have been described, but its potential role in improving DCM is less well characterized. We investigated the consequences of expressing a cardiac-specific transgene encoding locally acting IGF1 propeptide (muscle-produced IGF1; mIGF1) on disease progression in a mouse model of DCM [cardiac-specific and inducible serum response factor (<italic>SRF</italic>
) gene disruption] that mimics some forms of human DCM. Cardiac-specific mIGF1 expression substantially extended the lifespan of <italic>SRF</italic>
mutant mice, markedly improved cardiac functions, and delayed both DCM and HF. These protective effects were accompanied by an overall improvement in cardiomyocyte architecture and a massive reduction of myocardial fibrosis with a concomitant amelioration of inflammation. At least some of the beneficial effects of <italic>mIGF1</italic>
transgene expression were due to mIGF1 counteracting the strong increase in CTGF expression within cardiomyocytes caused by SRF deficiency, resulting in the blockade of fibroblast proliferation and related myocardial fibrosis. These findings demonstrate that SRF plays a key role in the modulation of cardiac fibrosis through repression of cardiomyocyte CTGF expression in a paracrine fashion. They also explain how impaired SRF function observed in human HF promotes fibrosis and adverse cardiac remodeling. Locally acting mIGF1 efficiently protects the myocardium from these adverse processes, and might thus represent a therapeutic avenue to counter DCM.</p>
</div>
</front>
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<pmc article-type="research-article"><pmc-dir>properties open_access</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-ta">Dis Model Mech</journal-id>
<journal-id journal-id-type="iso-abbrev">Dis Model Mech</journal-id>
<journal-id journal-id-type="hwp">dmm</journal-id>
<journal-id journal-id-type="publisher-id">DMM</journal-id>
<journal-title-group><journal-title>Disease Models & Mechanisms</journal-title>
</journal-title-group>
<issn pub-type="ppub">1754-8403</issn>
<issn pub-type="epub">1754-8411</issn>
<publisher><publisher-name>The Company of Biologists Limited</publisher-name>
</publisher>
</journal-meta>
<article-meta><article-id pub-id-type="pmid">22563064</article-id>
<article-id pub-id-type="pmc">3380711</article-id>
<article-id pub-id-type="doi">10.1242/dmm.009456</article-id>
<article-id pub-id-type="publisher-id">0050481</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject>
</subj-group>
</article-categories>
<title-group><article-title>Locally expressed IGF1 propeptide improves mouse heart function in induced dilated cardiomyopathy by blocking myocardial fibrosis and SRF-dependent CTGF induction</article-title>
</title-group>
<contrib-group><contrib contrib-type="author"><name><surname>Touvron</surname>
<given-names>Melissa</given-names>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
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<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
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<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<xref ref-type="aff" rid="af4-0050481"><sup>4</sup>
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<xref ref-type="aff" rid="af5-0050481"><sup>5</sup>
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<xref ref-type="aff" rid="af6-0050481"><sup>6</sup>
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<given-names>Mathias</given-names>
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<xref ref-type="aff" rid="af7-0050481"><sup>7</sup>
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<xref ref-type="aff" rid="af8-0050481"><sup>8</sup>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
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<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
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<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
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<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
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<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<given-names>Maria Paola</given-names>
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<xref ref-type="aff" rid="af9-0050481"><sup>9</sup>
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<xref ref-type="aff" rid="af9-0050481"><sup>9</sup>
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<xref ref-type="aff" rid="af10-0050481"><sup>10</sup>
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<xref ref-type="aff" rid="af11-0050481"><sup>11</sup>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
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<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
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<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<given-names>David</given-names>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
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<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
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<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<given-names>Jean-François</given-names>
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<xref ref-type="aff" rid="af1-0050481"><sup>1</sup>
</xref>
<xref ref-type="aff" rid="af2-0050481"><sup>2</sup>
</xref>
<xref ref-type="aff" rid="af3-0050481"><sup>3</sup>
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<xref ref-type="corresp" rid="c1"><sup>*</sup>
</xref>
</contrib>
</contrib-group>
<aff id="af1-0050481"><label>1</label>
INSERM, U1016, Institut Cochin, F-75014 Paris, France</aff>
<aff id="af2-0050481"><label>2</label>
CNRS, UMR8104, F-75014 Paris, France</aff>
<aff id="af3-0050481"><label>3</label>
Université Paris Descartes, F-75006 Paris, France</aff>
<aff id="af4-0050481"><label>4</label>
Faculté de Médecine Xavier-Bichat, F-75018 Paris, France</aff>
<aff id="af5-0050481"><label>5</label>
Université Paris 7, F-75013 Paris, France</aff>
<aff id="af6-0050481"><label>6</label>
INSERM, U872, F-75006 Paris, France</aff>
<aff id="af7-0050481"><label>7</label>
Université Paris 6, F-75006 Paris, France</aff>
<aff id="af8-0050481"><label>8</label>
CNRS, URA 4, F-75005 Paris, France</aff>
<aff id="af9-0050481"><label>9</label>
Heart Science Centre, National Heart and Lung Institute, Imperial College London, Harefield, Middlesex, UB9 6JH, UK</aff>
<aff id="af10-0050481"><label>10</label>
Mouse Biology Unit, European Molecular Biology Laboratory, Monterotondo, Rome, Italy</aff>
<aff id="af11-0050481"><label>11</label>
Australian Regenerative Medicine Institute/EMBL Australia, Monash University, Melbourne, VIC 3800, Australia</aff>
<author-notes><corresp id="c1"><label>*</label>
Author for correspondence (<email>jean-francois.decaux@inserm.fr</email>
)</corresp>
</author-notes>
<pub-date pub-type="ppub"><month>7</month>
<year>2012</year>
</pub-date>
<pub-date pub-type="epub"><day>5</day>
<month>4</month>
<year>2012</year>
</pub-date>
<volume>5</volume>
<issue>4</issue>
<fpage>481</fpage>
<lpage>491</lpage>
<history><date date-type="received"><day>19</day>
<month>12</month>
<year>2011</year>
</date>
<date date-type="accepted"><day>29</day>
<month>3</month>
<year>2012</year>
</date>
</history>
<permissions><copyright-statement>© 2012. Published by The Company of Biologists Ltd</copyright-statement>
<copyright-year>2012</copyright-year>
<license license-type="open-access"><license-p>This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by-nc-sa/3.0">http://creativecommons.org/licenses/by-nc-sa/3.0</ext-link>
), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms</license-p>
</license>
</permissions>
<self-uri content-type="pdf" xlink:type="simple" xlink:href="481.pdf"></self-uri>
<abstract><title>SUMMARY</title>
<p>Cardiac fibrosis is critically involved in the adverse remodeling accompanying dilated cardiomyopathies (DCMs), which leads to cardiac dysfunction and heart failure (HF). Connective tissue growth factor (CTGF), a profibrotic cytokine, plays a key role in this deleterious process. Some beneficial effects of IGF1 on cardiomyopathy have been described, but its potential role in improving DCM is less well characterized. We investigated the consequences of expressing a cardiac-specific transgene encoding locally acting IGF1 propeptide (muscle-produced IGF1; mIGF1) on disease progression in a mouse model of DCM [cardiac-specific and inducible serum response factor (<italic>SRF</italic>
) gene disruption] that mimics some forms of human DCM. Cardiac-specific mIGF1 expression substantially extended the lifespan of <italic>SRF</italic>
mutant mice, markedly improved cardiac functions, and delayed both DCM and HF. These protective effects were accompanied by an overall improvement in cardiomyocyte architecture and a massive reduction of myocardial fibrosis with a concomitant amelioration of inflammation. At least some of the beneficial effects of <italic>mIGF1</italic>
transgene expression were due to mIGF1 counteracting the strong increase in CTGF expression within cardiomyocytes caused by SRF deficiency, resulting in the blockade of fibroblast proliferation and related myocardial fibrosis. These findings demonstrate that SRF plays a key role in the modulation of cardiac fibrosis through repression of cardiomyocyte CTGF expression in a paracrine fashion. They also explain how impaired SRF function observed in human HF promotes fibrosis and adverse cardiac remodeling. Locally acting mIGF1 efficiently protects the myocardium from these adverse processes, and might thus represent a therapeutic avenue to counter DCM.</p>
</abstract>
<custom-meta-group><custom-meta><meta-name>special-property</meta-name>
<meta-value>TIB</meta-value>
</custom-meta>
</custom-meta-group>
</article-meta>
</front>
</pmc>
<affiliations><list><country><li>Australie</li>
<li>France</li>
<li>Italie</li>
<li>Royaume-Uni</li>
</country>
<region><li>Latium</li>
<li>Île-de-France</li>
</region>
<settlement><li>Paris</li>
<li>Rome</li>
</settlement>
<orgName><li>Université Paris-Descartes</li>
</orgName>
</list>
<tree><country name="France"><region name="Île-de-France"><name sortKey="Touvron, Melissa" sort="Touvron, Melissa" uniqKey="Touvron M" first="Melissa" last="Touvron">Melissa Touvron</name>
</region>
<name sortKey="Angelini, Aude" sort="Angelini, Aude" uniqKey="Angelini A" first="Aude" last="Angelini">Aude Angelini</name>
<name sortKey="Angelini, Aude" sort="Angelini, Aude" uniqKey="Angelini A" first="Aude" last="Angelini">Aude Angelini</name>
<name sortKey="Angelini, Aude" sort="Angelini, Aude" uniqKey="Angelini A" first="Aude" last="Angelini">Aude Angelini</name>
<name sortKey="Daegelen, Dominique" sort="Daegelen, Dominique" uniqKey="Daegelen D" first="Dominique" last="Daegelen">Dominique Daegelen</name>
<name sortKey="Daegelen, Dominique" sort="Daegelen, Dominique" uniqKey="Daegelen D" first="Dominique" last="Daegelen">Dominique Daegelen</name>
<name sortKey="Daegelen, Dominique" sort="Daegelen, Dominique" uniqKey="Daegelen D" first="Dominique" last="Daegelen">Dominique Daegelen</name>
<name sortKey="Decaux, Jean Francois" sort="Decaux, Jean Francois" uniqKey="Decaux J" first="Jean-François" last="Decaux">Jean-François Decaux</name>
<name sortKey="Decaux, Jean Francois" sort="Decaux, Jean Francois" uniqKey="Decaux J" first="Jean-François" last="Decaux">Jean-François Decaux</name>
<name sortKey="Decaux, Jean Francois" sort="Decaux, Jean Francois" uniqKey="Decaux J" first="Jean-François" last="Decaux">Jean-François Decaux</name>
<name sortKey="Escoubet, Brigitte" sort="Escoubet, Brigitte" uniqKey="Escoubet B" first="Brigitte" last="Escoubet">Brigitte Escoubet</name>
<name sortKey="Escoubet, Brigitte" sort="Escoubet, Brigitte" uniqKey="Escoubet B" first="Brigitte" last="Escoubet">Brigitte Escoubet</name>
<name sortKey="Escoubet, Brigitte" sort="Escoubet, Brigitte" uniqKey="Escoubet B" first="Brigitte" last="Escoubet">Brigitte Escoubet</name>
<name sortKey="Lamotte, Luciane" sort="Lamotte, Luciane" uniqKey="Lamotte L" first="Luciane" last="Lamotte">Luciane Lamotte</name>
<name sortKey="Lamotte, Luciane" sort="Lamotte, Luciane" uniqKey="Lamotte L" first="Luciane" last="Lamotte">Luciane Lamotte</name>
<name sortKey="Lamotte, Luciane" sort="Lamotte, Luciane" uniqKey="Lamotte L" first="Luciane" last="Lamotte">Luciane Lamotte</name>
<name sortKey="Mericskay, Mathias" sort="Mericskay, Mathias" uniqKey="Mericskay M" first="Mathias" last="Mericskay">Mathias Mericskay</name>
<name sortKey="Mericskay, Mathias" sort="Mericskay, Mathias" uniqKey="Mericskay M" first="Mathias" last="Mericskay">Mathias Mericskay</name>
<name sortKey="Touvron, Melissa" sort="Touvron, Melissa" uniqKey="Touvron M" first="Melissa" last="Touvron">Melissa Touvron</name>
<name sortKey="Touvron, Melissa" sort="Touvron, Melissa" uniqKey="Touvron M" first="Melissa" last="Touvron">Melissa Touvron</name>
<name sortKey="Tuil, David" sort="Tuil, David" uniqKey="Tuil D" first="David" last="Tuil">David Tuil</name>
<name sortKey="Tuil, David" sort="Tuil, David" uniqKey="Tuil D" first="David" last="Tuil">David Tuil</name>
<name sortKey="Tuil, David" sort="Tuil, David" uniqKey="Tuil D" first="David" last="Tuil">David Tuil</name>
</country>
<country name="Royaume-Uni"><noRegion><name sortKey="Santini, Maria Paola" sort="Santini, Maria Paola" uniqKey="Santini M" first="Maria Paola" last="Santini">Maria Paola Santini</name>
</noRegion>
<name sortKey="Rosenthal, Nadia" sort="Rosenthal, Nadia" uniqKey="Rosenthal N" first="Nadia" last="Rosenthal">Nadia Rosenthal</name>
</country>
<country name="Italie"><region name="Latium"><name sortKey="Rosenthal, Nadia" sort="Rosenthal, Nadia" uniqKey="Rosenthal N" first="Nadia" last="Rosenthal">Nadia Rosenthal</name>
</region>
</country>
<country name="Australie"><noRegion><name sortKey="Rosenthal, Nadia" sort="Rosenthal, Nadia" uniqKey="Rosenthal N" first="Nadia" last="Rosenthal">Nadia Rosenthal</name>
</noRegion>
</country>
</tree>
</affiliations>
</record>
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