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dc.contributor.authorSager, Hendrik B.
dc.contributor.authorHeidt, Timo
dc.contributor.authorHulsmans, Maarten
dc.contributor.authorDutta, Partha
dc.contributor.authorCourties, Gabriel P
dc.contributor.authorSebas, Matthew
dc.contributor.authorWojtkiewicz, Gregory R.
dc.contributor.authorTricot, Benoit
dc.contributor.authorIwamoto, Yoshiko
dc.contributor.authorSun, Yuan
dc.contributor.authorWeissleder, Ralph
dc.contributor.authorLibby, Peter
dc.contributor.authorSwirski, Filip K.
dc.contributor.authorNahrendorf, Matthias
dc.date.accessioned2015-11-23T19:06:06Z
dc.date.issued2015
dc.identifier.citationSager, Hendrik B., Timo Heidt, Maarten Hulsmans, Partha Dutta, Gabriel Courties, Matthew Sebas, Gregory R. Wojtkiewicz, et al. 2015. “Targeting Interleukin-1? Reduces Leukocyte Production After Acute Myocardial Infarction.” Circulation (September 10): CIRCULATIONAHA.115.016160. doi:10.1161/circulationaha.115.016160.en_US
dc.identifier.issn0009-7322en_US
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:23606068
dc.description.abstractBackground—Myocardial infarction (MI) is an ischemic wound that recruits millions of leukocytes. MI-associated blood leukocytosis correlates inversely with patient survival, yet the signals driving heightened leukocyte production after MI remain incompletely understood. Methods and Results—With the use of parabiosis surgery, this study shows that soluble danger signals, among them interleukin-1β, increase bone marrow hematopoietic stem cell proliferation after MI. Data obtained in bone marrow reconstitution experiments reveal that interleukin-1β enhances hematopoietic stem cell proliferation by both direct actions on hematopoietic cells and through modulation of the bone marrow’s hematopoietic microenvironment. An antibody that neutralizes interleukin-1β suppresses these effects. Anti-interleukin-1β treatment dampens the post-MI increase in hematopoietic stem cell proliferation. Consequently, decreased leukocyte numbers in the blood and infarct reduce inflammation and diminish post-MI heart failure in ApoE–/– mice with atherosclerosis. Conclusions—The presented insight into post-MI bone marrow activation identifies a mechanistic target for muting inflammation in the ischemically damaged heart.en_US
dc.language.isoen_USen_US
dc.publisherOvid Technologies (Wolters Kluwer Health)en_US
dc.relation.isversionof10.1161/CIRCULATIONAHA.115.016160en_US
dash.licenseOAP
dc.subjecthematopoiesisen_US
dc.subjecthematopoietic stem cellsen_US
dc.subjectinterleukin-1βen_US
dc.subjectmyocardial infarctionen_US
dc.titleTargeting Interleukin-1β Reduces Leukocyte Production After Acute Myocardial Infarctionen_US
dc.typeJournal Articleen_US
dc.description.versionAccepted Manuscripten_US
dc.relation.journalCirculationen_US
dash.depositing.authorLibby, Peter
dc.date.available2015-11-23T19:06:06Z
dc.identifier.doi10.1161/CIRCULATIONAHA.115.016160*
dash.authorsorderedfalse
dash.contributor.affiliatedDutta, Partha
dash.contributor.affiliatedCourties, Gabriel
dash.contributor.affiliatedHulsmans, Maarten
dash.contributor.affiliatedSwirski, Filip
dash.contributor.affiliatedNahrendorf, Matthias
dash.contributor.affiliatedWeissleder, Ralph
dash.contributor.affiliatedLibby, Peter


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