SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS
Identifieur interne : 000222 ( Istex/Curation ); précédent : 000221; suivant : 000223SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS
Auteurs : G. Y. Oudit [Canada] ; Z. Kassiri [Canada] ; C. Jiang [République populaire de Chine] ; P. P. Liu [Canada] ; S. M. Poutanen [Canada] ; J. M. Penninger [Autriche] ; J. Butany [Canada]Source :
- European Journal of Clinical Investigation [ 0014-2972 ] ; 2009-07.
English descriptors
- Teeft :
- Ace2, Ace2 expression, Ace2 mrna, Ace2 protein expression, Alberta, Angiotensin, Angiotensinconverting enzyme, Bacterial pneumonia, Butany, Cardiac disease, Clinical investigation, Clinical investigation journal foundation ace2, Coronavirus, Diastolic dysfunction, Dysfunction, European journal, Functional receptor, Heart disease, Heart samples, Journal compilation, Kassiri, Macrophage, Mrna, Murine model, Myocardial, Myocardial ace2 mrna, Myocardial ace2 mrna expression, Myocardial ace2 protein levels, Myocardial damage, Myocardial infection, Myocarditis, Other groups, Oudit, Pulmonary infection, Receptor, Respiratory syndrome, Sars, Sars crisis, Sarscov, Sepsis, Stichting european society, Syndrome, University health network, Western blot analysis.
Abstract
Background 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. Materials and methods 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. Results 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. Conclusions 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.
Url:
DOI: 10.1111/j.1365-2362.2009.02153.x
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Kassiri</name><affiliation wicri:level="1"><mods:affiliation>University of Alberta, Edmonton, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>University of Alberta, Edmonton</wicri:regionArea></affiliation></author><author><name sortKey="Jiang, C" sort="Jiang, C" uniqKey="Jiang C" first="C." last="Jiang">C. Jiang</name><affiliation wicri:level="1"><mods:affiliation>Peking Union Medical College, Beijing, China</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Peking Union Medical College, Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Liu, P P" sort="Liu, P P" uniqKey="Liu P" first="P. P." last="Liu">P. P. 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Y." last="Oudit">G. Y. Oudit</name><affiliation wicri:level="1"><mods:affiliation>University of Alberta, Edmonton, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>University of Alberta, Edmonton</wicri:regionArea></affiliation></author><author><name sortKey="Kassiri, Z" sort="Kassiri, Z" uniqKey="Kassiri Z" first="Z." last="Kassiri">Z. Kassiri</name><affiliation wicri:level="1"><mods:affiliation>University of Alberta, Edmonton, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>University of Alberta, Edmonton</wicri:regionArea></affiliation></author><author><name sortKey="Jiang, C" sort="Jiang, C" uniqKey="Jiang C" first="C." last="Jiang">C. Jiang</name><affiliation wicri:level="1"><mods:affiliation>Peking Union Medical College, Beijing, China</mods:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Peking Union Medical College, Beijing</wicri:regionArea></affiliation></author><author><name sortKey="Liu, P P" sort="Liu, P P" uniqKey="Liu P" first="P. P." last="Liu">P. P. Liu</name><affiliation wicri:level="1"><mods:affiliation>University Health Network, University of Toronto, Toronto, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>University Health Network, University of Toronto, Toronto</wicri:regionArea></affiliation></author><author><name sortKey="Poutanen, S M" sort="Poutanen, S M" uniqKey="Poutanen S" first="S. M." last="Poutanen">S. M. Poutanen</name><affiliation wicri:level="1"><mods:affiliation>Mount Sinai Hospital, Toronto, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Mount Sinai Hospital, Toronto</wicri:regionArea></affiliation></author><author><name sortKey="Penninger, J M" sort="Penninger, J M" uniqKey="Penninger J" first="J. M." last="Penninger">J. M. Penninger</name><affiliation wicri:level="1"><mods:affiliation>Institute for Molecular Biotechnology of the Austrian Academy of Sciences, Vienna, Austria</mods:affiliation><country xml:lang="fr">Autriche</country><wicri:regionArea>Institute for Molecular Biotechnology of the Austrian Academy of Sciences, Vienna</wicri:regionArea></affiliation></author><author><name sortKey="Butany, J" sort="Butany, J" uniqKey="Butany J" first="J." last="Butany">J. Butany</name><affiliation wicri:level="1"><mods:affiliation>University Health Network, University of Toronto, Toronto, Canada</mods:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>University Health Network, University of Toronto, Toronto</wicri:regionArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">European Journal of Clinical Investigation</title><title level="j" type="alt">EUROPEAN JOURNAL OF CLINICAL INVESTIGATION</title><idno type="ISSN">0014-2972</idno><idno type="eISSN">1365-2362</idno><imprint><biblScope unit="vol">39</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="618">618</biblScope><biblScope unit="page" to="625">625</biblScope><biblScope unit="page-count">8</biblScope><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="2009-07">2009-07</date></imprint><idno type="ISSN">0014-2972</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Ace2</term><term>Ace2 expression</term><term>Ace2 mrna</term><term>Ace2 protein expression</term><term>Alberta</term><term>Angiotensin</term><term>Angiotensinconverting enzyme</term><term>Bacterial pneumonia</term><term>Butany</term><term>Cardiac disease</term><term>Clinical investigation</term><term>Clinical investigation journal foundation ace2</term><term>Coronavirus</term><term>Diastolic dysfunction</term><term>Dysfunction</term><term>European journal</term><term>Functional receptor</term><term>Heart disease</term><term>Heart samples</term><term>Journal compilation</term><term>Kassiri</term><term>Macrophage</term><term>Mrna</term><term>Murine model</term><term>Myocardial</term><term>Myocardial ace2 mrna</term><term>Myocardial ace2 mrna expression</term><term>Myocardial ace2 protein levels</term><term>Myocardial damage</term><term>Myocardial infection</term><term>Myocarditis</term><term>Other groups</term><term>Oudit</term><term>Pulmonary infection</term><term>Receptor</term><term>Respiratory syndrome</term><term>Sars</term><term>Sars crisis</term><term>Sarscov</term><term>Sepsis</term><term>Stichting european society</term><term>Syndrome</term><term>University health network</term><term>Western blot analysis</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Background 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. Materials and methods 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. Results 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. Conclusions 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.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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