SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS
Identifieur interne : 000C72 ( Pmc/Checkpoint ); précédent : 000C71; suivant : 000C73SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS
Auteurs : G. Y. Oudit ; Z. Kassiri ; C. Jiang ; P. P. Liu ; S. M. Poutanen ; J. M. Penninger ; J. ButanySource :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 2009.
Abstract
Url:
DOI: 10.1111/j.1365-2362.2009.02153.x
PubMed: 19453650
PubMed Central: 7163766
Affiliations:
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<series><title level="j">European Journal of Clinical Investigation</title>
<idno type="ISSN">0014-2972</idno>
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<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<p><bold>Background </bold>
Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1–7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction.</p>
<p><bold>Materials and methods </bold>
We studied mice infected with the human strain of the SARS‐CoV and encephalomyocarditis virus and examined ACE2 mRNA and protein expression. Autopsy heart samples from patients who succumbed to the SARS crisis in Toronto (Canada) were used to investigate the impact of SARS on myocardial structure, inflammation and ACE2 protein expression.</p>
<p><bold>Results </bold>
Pulmonary infection with the human SARS‐CoV in mice led to an ACE2‐dependent myocardial infection with a marked decrease in ACE2 expression confirming a critical role of ACE2 in mediating SARS‐CoV infection in the heart. The SARS‐CoV viral RNA was detected in 35% (7/20) of autopsied human heart samples obtained from patients who succumbed to the SARS crisis during the Toronto SARS outbreak. Macrophage‐specific staining showed a marked increase in macrophage infiltration with evidence of myocardial damage in patients who had SARS‐CoV in their hearts. The presence of SARS‐CoV in the heart was also associated with marked reductions in ACE2 protein expression.</p>
<p><bold>Conclusions </bold>
Our data show that SARS‐CoV can mediate myocardial inflammation and damage associated with down‐regulation of myocardial ACE2 system, which may be responsible for the myocardial dysfunction and adverse cardiac outcomes in patients with SARS.</p>
</div>
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<front><journal-meta><journal-id journal-id-type="nlm-ta">Eur J Clin Invest</journal-id>
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<journal-id journal-id-type="doi">10.1111/(ISSN)1365-2362</journal-id>
<journal-id journal-id-type="publisher-id">ECI</journal-id>
<journal-title-group><journal-title>European Journal of Clinical Investigation</journal-title>
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<issn pub-type="ppub">0014-2972</issn>
<issn pub-type="epub">1365-2362</issn>
<publisher><publisher-name>Blackwell Publishing Ltd</publisher-name>
<publisher-loc>Oxford, UK</publisher-loc>
</publisher>
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<article-meta><article-id pub-id-type="pmid">19453650</article-id>
<article-id pub-id-type="pmc">7163766</article-id>
<article-id pub-id-type="doi">10.1111/j.1365-2362.2009.02153.x</article-id>
<article-id pub-id-type="publisher-id">ECI2153</article-id>
<article-categories><subj-group subj-group-type="heading"><subject>Short Report</subject>
</subj-group>
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<title-group><article-title>SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS</article-title>
<alt-title alt-title-type="left-running-head">G. Y. OUDIT <italic>ET AL.</italic>
</alt-title>
<alt-title alt-title-type="right-running-head">ACE2, HEART DISEASE AND SEVERE ACUTE RESPIRATORY SYNDROME</alt-title>
</title-group>
<contrib-group><contrib id="cr1" contrib-type="author"><name><surname>Oudit</surname>
<given-names>G. Y.</given-names>
</name>
<xref ref-type="aff" rid="a1"><sup>1</sup>
</xref>
<xref ref-type="author-notes" rid="fn1"><sup>1</sup>
</xref>
</contrib>
<contrib id="cr2" contrib-type="author"><name><surname>Kassiri</surname>
<given-names>Z.</given-names>
</name>
<xref ref-type="aff" rid="a1"><sup>1</sup>
</xref>
</contrib>
<contrib id="cr3" contrib-type="author"><name><surname>Jiang</surname>
<given-names>C.</given-names>
</name>
<xref ref-type="aff" rid="a2"><sup>2</sup>
</xref>
</contrib>
<contrib id="cr4" contrib-type="author"><name><surname>Liu</surname>
<given-names>P. P.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
</xref>
</contrib>
<contrib id="cr5" contrib-type="author"><name><surname>Poutanen</surname>
<given-names>S. M.</given-names>
</name>
<xref ref-type="aff" rid="a4"><sup>4</sup>
</xref>
</contrib>
<contrib id="cr6" contrib-type="author"><name><surname>Penninger</surname>
<given-names>J. M.</given-names>
</name>
<xref ref-type="aff" rid="a5"><sup>5</sup>
</xref>
</contrib>
<contrib id="cr7" contrib-type="author"><name><surname>Butany</surname>
<given-names>J.</given-names>
</name>
<xref ref-type="aff" rid="a3"><sup>3</sup>
</xref>
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<aff id="a1"><label><sup>1</sup>
</label>
University of Alberta, Edmonton, Canada</aff>
<aff id="a2"><label><sup>2</sup>
</label>
Peking Union Medical College, Beijing, China</aff>
<aff id="a3"><label><sup>3</sup>
</label>
University Health Network, University of Toronto, Toronto, Canada</aff>
<aff id="a4"><label><sup>4</sup>
</label>
Mount Sinai Hospital, Toronto, Canada</aff>
<aff id="a5"><label><sup>5</sup>
</label>
Institute for Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria</aff>
<author-notes><corresp id="correspondenceTo">Gavin Y. Oudit, MD, PhD, FRCPC, Division of Cardiology, Department of Medicine, Mazankowski Alberta Heart Institute, University of Alberta, HMRC‐474, Edmonton, AB, T6G 2S2, Canada. Tel.: 780‐407‐8569; fax: 780‐407‐6452; e‐mail: <email>gavin.oudit@ualberta.ca</email>
</corresp>
<fn id="fn1"><label>1</label>
<p>Clinician‐Investigator of the Alberta Heritage Foundation for Medical Research.</p>
</fn>
</author-notes>
<pub-date pub-type="epub"><day>06</day>
<month>5</month>
<year>2009</year>
</pub-date>
<pub-date pub-type="ppub"><month>7</month>
<year>2009</year>
</pub-date>
<volume>39</volume>
<issue>7</issue>
<issue-id pub-id-type="doi">10.1111/eci.2009.39.issue-7</issue-id>
<fpage>618</fpage>
<lpage>625</lpage>
<history><pmc-comment>supplied string: Received 27 January 2009; accepted 6 April 2009</pmc-comment>
<date date-type="received"><day>27</day>
<month>1</month>
<year>2009</year>
</date>
<date date-type="accepted"><day>6</day>
<month>4</month>
<year>2009</year>
</date>
</history>
<permissions><copyright-statement content-type="article-copyright">© 2009 The Authors. Journal Compilation © 2009 Stichting European Society for Clinical Investigation Journal Foundation</copyright-statement>
<license><license-p>This article is being made freely available through PubMed Central as part of the COVID-19 public health emergency response. It can be used for unrestricted research re-use and analysis in any form or by any means with acknowledgement of the original source, for the duration of the public health emergency.</license-p>
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<self-uri content-type="pdf" xlink:href="file:ECI-39-618.pdf"></self-uri>
<abstract><title>Abstract</title>
<p><bold>Background </bold>
Angiotensin converting enzyme 2 (ACE2), a monocarboxylase that degrades angiotensin II to angiotensin 1–7, is also the functional receptor for severe acute respiratory syndrome (SARS) coronavirus (SARS‐CoV) and is highly expressed in the lungs and heart. Patients with SARS also suffered from cardiac disease including arrhythmias, sudden cardiac death, and systolic and diastolic dysfunction.</p>
<p><bold>Materials and methods </bold>
We studied mice infected with the human strain of the SARS‐CoV and encephalomyocarditis virus and examined ACE2 mRNA and protein expression. Autopsy heart samples from patients who succumbed to the SARS crisis in Toronto (Canada) were used to investigate the impact of SARS on myocardial structure, inflammation and ACE2 protein expression.</p>
<p><bold>Results </bold>
Pulmonary infection with the human SARS‐CoV in mice led to an ACE2‐dependent myocardial infection with a marked decrease in ACE2 expression confirming a critical role of ACE2 in mediating SARS‐CoV infection in the heart. The SARS‐CoV viral RNA was detected in 35% (7/20) of autopsied human heart samples obtained from patients who succumbed to the SARS crisis during the Toronto SARS outbreak. Macrophage‐specific staining showed a marked increase in macrophage infiltration with evidence of myocardial damage in patients who had SARS‐CoV in their hearts. The presence of SARS‐CoV in the heart was also associated with marked reductions in ACE2 protein expression.</p>
<p><bold>Conclusions </bold>
Our data show that SARS‐CoV can mediate myocardial inflammation and damage associated with down‐regulation of myocardial ACE2 system, which may be responsible for the myocardial dysfunction and adverse cardiac outcomes in patients with SARS.</p>
</abstract>
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<tree><noCountry><name sortKey="Butany, J" sort="Butany, J" uniqKey="Butany J" first="J." last="Butany">J. Butany</name>
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<name sortKey="Kassiri, Z" sort="Kassiri, Z" uniqKey="Kassiri Z" first="Z." last="Kassiri">Z. Kassiri</name>
<name sortKey="Liu, P P" sort="Liu, P P" uniqKey="Liu P" first="P. P." last="Liu">P. P. Liu</name>
<name sortKey="Oudit, G Y" sort="Oudit, G Y" uniqKey="Oudit G" first="G. Y." last="Oudit">G. Y. Oudit</name>
<name sortKey="Penninger, J M" sort="Penninger, J M" uniqKey="Penninger J" first="J. M." last="Penninger">J. M. Penninger</name>
<name sortKey="Poutanen, S M" sort="Poutanen, S M" uniqKey="Poutanen S" first="S. M." last="Poutanen">S. M. Poutanen</name>
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