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dc.contributor.authorRickard, AJ
dc.contributor.authorMorgan, J
dc.contributor.authorBienvenu, LA
dc.contributor.authorFletcher, EK
dc.contributor.authorCranston, GA
dc.contributor.authorShen, JZ
dc.contributor.authorReichelt, ME
dc.contributor.authorDelbridge, LM
dc.contributor.authorYoung, MJ
dc.date.available2014-05-22T07:11:06Z
dc.date.issued2012-12-01
dc.identifierpii: HYPERTENSIONAHA.112.203158
dc.identifier.citationRickard, A. J., Morgan, J., Bienvenu, L. A., Fletcher, E. K., Cranston, G. A., Shen, J. Z., Reichelt, M. E., Delbridge, L. M. & Young, M. J. (2012). Cardiomyocyte Mineralocorticoid Receptors Are Essential for Deoxycorticosterone/Salt-Mediated Inflammation and Cardiac Fibrosis. HYPERTENSION, 60 (6), pp.1443-U194. https://doi.org/10.1161/HYPERTENSIONAHA.112.203158.
dc.identifier.issn0194-911X
dc.identifier.urihttp://hdl.handle.net/11343/32826
dc.descriptionC1 - Journal Articles Refereed
dc.description.abstractBecause the role of mineralocorticoid receptors in specific cell types in cardiac remodeling remains unknown, we have compared cardiac responses with deoxycorticosterone/salt in cardiomyocyte mineralocorticoid receptor-null (MyoMRKO) and wild-type (WT) mice at 8 days and 8 weeks. No differences in cardiac function between untreated WT and MyoMRKO mice were found, whereas profibrotic markers were reduced in MyoMRKO hearts at baseline. At 8 days, MyoMRKO showed monocyte/macrophage recruitment equivalent to WT mice in response to deoxycorticosterone/salt but a suppression of markers of fibrosis compared with WT. At 8 weeks, MyoMRKO mice showed no deoxycorticosterone/salt-induced increase in inflammatory cell infiltration and collagen deposition or in proinflammatory gene expression. Although some profibrotic markers were equivalently increased in both genotypes, MyoMRKO mice also showed increased baseline levels of mRNA and protein for the transforming growth factor-β/connective tissue growth factor inhibitor decorin compared with WT that was accompanied by higher levels of matrix metalloproteinase 2/matrix metalloproteinase 9 activity. These data point to a direct role for cardiomyocyte mineralocorticoid receptor in both deoxycorticosterone/salt-induced tissue inflammation and remodeling and suggest potential mechanisms for the cardioprotective effects of selective mineralocorticoid receptor blockade in cardiomyocytes that may involve regulation of matrix metalloproteinase 2/matrix metalloproteinase 9 activity and the transforming growth factor-β-connective tissue growth factor profibrotic pathway.
dc.languageEnglish
dc.publisherLIPPINCOTT WILLIAMS & WILKINS
dc.subjectCardiology (incl. Cardiovascular Diseases); Cardiovascular System and Diseases
dc.titleCardiomyocyte Mineralocorticoid Receptors Are Essential for Deoxycorticosterone/Salt-Mediated Inflammation and Cardiac Fibrosis
dc.typeJournal Article
dc.identifier.doi10.1161/HYPERTENSIONAHA.112.203158
melbourne.peerreviewPeer Reviewed
melbourne.affiliationThe University of Melbourne
melbourne.affiliation.departmentPhysiology
melbourne.source.titleHYPERTENSION
melbourne.source.volume60
melbourne.source.issue6
melbourne.source.pages1443-U194
dc.research.codefor110201
dc.research.codeseo2008920103
melbourne.publicationid188383
melbourne.elementsid498316
melbourne.contributor.authorBienvenu, Laura
melbourne.contributor.authorREICHELT, MELISSA
melbourne.contributor.authorDelbridge, Leanne
dc.identifier.eissn1524-4563
melbourne.fieldofresearch320101 Cardiology (incl. cardiovascular diseases)
melbourne.seocode200199 Clinical health not elsewhere classified
melbourne.accessrightsThis item is currently not available from this repository


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