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Age-related differential structural and transcriptomic responses in the hypertensive heart

Marques, Francine Z., Chu, Po-Yin, Ziemann, Mark, Kaspi, Antony, Kiriazis, Helen, Du, Xiao-Jun, El-Osta, Assam and Kaye, David M. 2018, Age-related differential structural and transcriptomic responses in the hypertensive heart, Frontiers in physiology, vol. 9, pp. 1-13, doi: 10.3389/fphys.2018.00817.

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Title Age-related differential structural and transcriptomic responses in the hypertensive heart
Author(s) Marques, Francine Z.
Chu, Po-Yin
Ziemann, MarkORCID iD for Ziemann, Mark orcid.org/0000-0002-7688-6974
Kaspi, Antony
Kiriazis, Helen
Du, Xiao-Jun
El-Osta, Assam
Kaye, David M.
Journal name Frontiers in physiology
Volume number 9
Article ID 817
Start page 1
End page 13
Total pages 13
Publisher Frontiers
Place of publication Lausanne, Switzerland
Publication date 2018-07-09
ISSN 1664-042X
Keyword(s) heart failure
aging
fibrosis
microRNAs
miRNAs
miRs
transcriptome
pathways
Summary While aging is a critical risk factor for heart failure, it remains uncertain whether the aging heart responds differentially to a hypertensive stimuli. Here we investigated phenotypic and transcriptomic differences between the young and aging heart using a mineralocorticoid-excess model of hypertension. Ten-week ("young") and 36-week ("aging") mice underwent a unilateral uninephrectomy with deoxycorticosterone acetate (DOCA) pellet implantation (n = 6-8/group) and were followed for 6 weeks. Cardiac structure and function, blood pressure (BP) and the cardiac transcriptome were subsequently examined. Young and aging DOCA mice had high BP, increased cardiac mass, cardiac hypertrophy, and fibrosis. Left ventricular end-diastolic pressure increased in aging DOCA-treated mice in contrast to young DOCA mice. Interstitial and perivascular fibrosis occurred in response to DOCA, but perivascular fibrosis was greater in aging mice. Transcriptomic analysis showed that young mice had features of higher oxidative stress, likely due to activation of the respiratory electron transport chain. In contrast, aging mice showed up-regulation of collagen formation in association with activation of innate immunity together with markers of inflammation including cytokine and platelet signaling. In comparison to younger mice, aging mice demonstrated different phenotypic and molecular responses to hypertensive stress. These findings have potential implications for the pathogenesis of age-related forms of cardiovascular disease, particularly heart failure.
Language eng
DOI 10.3389/fphys.2018.00817
HERDC Research category C1.1 Refereed article in a scholarly journal
ERA Research output type C Journal article
Copyright notice ©2018, Marques, Chu, Ziemann, Kaspi, Kiriazis, Du, El-Osta and Kaye.
Free to Read? Yes
Use Rights Creative Commons Attribution licence
Persistent URL http://hdl.handle.net/10536/DRO/DU:30113078

Document type: Journal Article
Collections: School of Life and Environmental Sciences
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Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact drosupport@deakin.edu.au.