SARS‐coronavirus modulation of myocardial ACE2 expression and inflammation in patients with SARS
Identifieur interne : 002D07 ( Main/Exploration ); précédent : 002D06; suivant : 002D08SARS‐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.
Descripteurs français
- KwdFr :
- Activation virale, Animaux, Autopsie, Humains, Immunohistochimie, Maladies cardiovasculaires (), Maladies cardiovasculaires (virologie), Myocarde (anatomopathologie), Mâle, Peptidyl-Dipeptidase A (génétique), Peptidyl-Dipeptidase A (métabolisme), Régulation négative, Souris, Virus du SRAS (génétique), Virus du SRAS (métabolisme).
- MESH :
- anatomopathologie : Myocarde.
- génétique : Peptidyl-Dipeptidase A, Virus du SRAS.
- métabolisme : Peptidyl-Dipeptidase A, Virus du SRAS.
- virologie : Maladies cardiovasculaires.
- Pascal (Inist)
- MESH :
- Wicri :
English descriptors
- KwdEn :
- Animals, Autopsy, Cardiovascular Diseases (prevention & control), Cardiovascular Diseases (virology), Coronavirus, Down-Regulation, Heart, Human, Humans, Immunohistochemistry, Inflammation, Macrophage, Male, Medicine, Mice, Modulation, Myocardium, Myocardium (pathology), Patient, Peptidyl-Dipeptidase A (genetics), Peptidyl-Dipeptidase A (metabolism), Peptidyl-dipeptidase A, SARS Virus (genetics), SARS Virus (metabolism), Severe acute respiratory syndrome, Virus Activation.
- MESH :
- chemical , genetics : Peptidyl-Dipeptidase A.
- chemical , metabolism : Peptidyl-Dipeptidase A.
- genetics : SARS Virus.
- metabolism : SARS Virus.
- pathology : Myocardium.
- prevention & control : Cardiovascular Diseases.
- virology : Cardiovascular Diseases.
- Teeft :
- Ace2, Ace2 expression, Ace2 mrna, Ace2 protein expression, Alberta, Angiotensin, Angiotensinconverting enzyme, Animals, Autopsy, Bacterial pneumonia, Butany, Cardiac disease, Clinical investigation, Clinical investigation journal foundation ace2, Coronavirus, Diastolic dysfunction, Down-Regulation, Dysfunction, European journal, Functional receptor, Heart disease, Heart samples, Humans, Immunohistochemistry, Journal compilation, Kassiri, Macrophage, Male, Mice, 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, Virus Activation, 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:
- https://api.istex.fr/ark:/67375/WNG-PJKHPTV8-F/fulltext.pdf
- http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7163766
DOI: 10.1111/j.1365-2362.2009.02153.x
Affiliations:
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Y." last="Oudit">G. Y. Oudit</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>University of Alberta, Edmonton</wicri:regionArea><wicri:noRegion>Edmonton</wicri:noRegion></affiliation></author><author><name sortKey="Kassiri, Z" sort="Kassiri, Z" uniqKey="Kassiri Z" first="Z." last="Kassiri">Z. Kassiri</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>University of Alberta, Edmonton</wicri:regionArea><wicri:noRegion>Edmonton</wicri:noRegion></affiliation></author><author><name sortKey="Jiang, C" sort="Jiang, C" uniqKey="Jiang C" first="C." last="Jiang">C. Jiang</name><affiliation wicri:level="3"><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>Peking Union Medical College, Beijing</wicri:regionArea><placeName><settlement type="city">Pékin</settlement></placeName></affiliation></author><author><name sortKey="Liu, P P" sort="Liu, P P" uniqKey="Liu P" first="P. 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type="ISSN">0014-2972</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Autopsy</term><term>Cardiovascular Diseases (prevention & control)</term><term>Cardiovascular Diseases (virology)</term><term>Coronavirus</term><term>Down-Regulation</term><term>Heart</term><term>Human</term><term>Humans</term><term>Immunohistochemistry</term><term>Inflammation</term><term>Macrophage</term><term>Male</term><term>Medicine</term><term>Mice</term><term>Modulation</term><term>Myocardium</term><term>Myocardium (pathology)</term><term>Patient</term><term>Peptidyl-Dipeptidase A (genetics)</term><term>Peptidyl-Dipeptidase A (metabolism)</term><term>Peptidyl-dipeptidase A</term><term>SARS Virus (genetics)</term><term>SARS Virus (metabolism)</term><term>Severe acute respiratory syndrome</term><term>Virus Activation</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Activation virale</term><term>Animaux</term><term>Autopsie</term><term>Humains</term><term>Immunohistochimie</term><term>Maladies cardiovasculaires ()</term><term>Maladies cardiovasculaires (virologie)</term><term>Myocarde (anatomopathologie)</term><term>Mâle</term><term>Peptidyl-Dipeptidase A (génétique)</term><term>Peptidyl-Dipeptidase A (métabolisme)</term><term>Régulation négative</term><term>Souris</term><term>Virus du SRAS (génétique)</term><term>Virus du SRAS (métabolisme)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Peptidyl-Dipeptidase A</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Myocarde</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Peptidyl-Dipeptidase A</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Myocardium</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Maladies cardiovasculaires</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Angiotensin converting enzyme</term><term>Coeur</term><term>Coronavirus</term><term>Homme</term><term>Inflammation</term><term>Macrophage</term><term>Malade</term><term>Modulation</term><term>Myocarde</term><term>Médecine</term><term>Peptidyl-dipeptidase A</term><term>Syndrome respiratoire aigu sévère</term></keywords><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>Animals</term><term>Autopsy</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>Down-Regulation</term><term>Dysfunction</term><term>European journal</term><term>Functional receptor</term><term>Heart disease</term><term>Heart samples</term><term>Humans</term><term>Immunohistochemistry</term><term>Journal compilation</term><term>Kassiri</term><term>Macrophage</term><term>Male</term><term>Mice</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>Virus Activation</term><term>Western blot analysis</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Activation virale</term><term>Animaux</term><term>Autopsie</term><term>Humains</term><term>Immunohistochimie</term><term>Maladies cardiovasculaires</term><term>Mâle</term><term>Régulation négative</term><term>Souris</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term><term>Médecine</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><affiliations><list><country><li>Autriche</li><li>Canada</li><li>République populaire de Chine</li></country><region><li>Vienne (Autriche)</li></region><settlement><li>Pékin</li><li>Vienne (Autriche)</li></settlement></list><tree><country name="Canada"><noRegion><name sortKey="Oudit, G Y" sort="Oudit, G Y" uniqKey="Oudit G" first="G. Y." last="Oudit">G. Y. Oudit</name></noRegion><name sortKey="Butany, J" sort="Butany, J" uniqKey="Butany J" first="J." last="Butany">J. Butany</name><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="Poutanen, S M" sort="Poutanen, S M" uniqKey="Poutanen S" first="S. M." last="Poutanen">S. M. Poutanen</name></country><country name="République populaire de Chine"><noRegion><name sortKey="Jiang, C" sort="Jiang, C" uniqKey="Jiang C" first="C." last="Jiang">C. Jiang</name></noRegion></country><country name="Autriche"><region name="Vienne (Autriche)"><name sortKey="Penninger, J M" sort="Penninger, J M" uniqKey="Penninger J" first="J. M." last="Penninger">J. M. Penninger</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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