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Caloric restriction ameliorates angiotensin II-induced mitochondrial remodeling and cardiac hypertrophy
Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
Institute of Biomedicine, University of Helsinki, Helsinki, Finland.
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2012 (English)In: Hypertension, ISSN 0194-911X, E-ISSN 1524-4563, Vol. 59, no 1, p. 76-84Article in journal (Refereed) Published
Abstract [en]

Angiotensin II-induced cardiac damage is associated with oxidative stress-dependent mitochondrial dysfunction. Caloric restriction (CR), a dietary regimen that increases mitochondrial activity and cellular stress resistance, could provide protection. We tested that hypothesis in double transgenic rats harboring human renin and angiotensinogen genes (dTGRs). CR (60% of energy intake for 4 weeks) decreased mortality in dTGRs. CR ameliorated angiotensin II-induced cardiomyocyte hypertrophy, vascular inflammation, cardiac damage and fibrosis, cardiomyocyte apoptosis, and cardiac atrial natriuretic peptide mRNA overexpression. The effects were blood pressure independent and were linked to increased endoplasmic reticulum stress, autophagy, serum adiponectin level, and 5' AMP-activated protein kinase phosphorylation. CR decreased cardiac p38 phosphorylation, nitrotyrosine expression, and serum insulin-like growth factor 1 levels. Mitochondria from dTGR hearts showed clustered mitochondrial patterns, decreased numbers, and volume fractions but increased trans-sectional areas. All of these effects were reduced in CR dTGRs. Mitochondrial proteomic profiling identified 43 dTGR proteins and 42 Sprague-Dawley proteins, of which 29 proteins were in common in response to CR. We identified 7 proteins in CR dTGRs that were not found in control dTGRs. In contrast, 6 mitochondrial proteins were identified from dTGRs that were not detected in any other group. Gene ontology annotations with the Panther protein classification system revealed downregulation of cytoskeletal proteins and enzyme modulators and upregulation of oxidoreductase activity in dTGRs. CR provides powerful, blood pressure-independent, protection against angiotensin II-induced mitochondrial remodeling and cardiac hypertrophy. The findings support the notion of modulating cardiac bioenergetics to ameliorate angiotensin II-induced cardiovascular complications.

Place, publisher, year, edition, pages
Lippincott Williams & Wilkins, 2012. Vol. 59, no 1, p. 76-84
National Category
Biochemistry and Molecular Biology Cardiac and Cardiovascular Systems
Identifiers
URN: urn:nbn:se:oru:diva-63660DOI: 10.1161/HYPERTENSIONAHA.111.179457ISI: 000298403800017PubMedID: 22068868Scopus ID: 2-s2.0-83655167120OAI: oai:DiVA.org:oru-63660DiVA, id: diva2:1169223
Funder
Academy of Finland
Note

Funding agencies:

Sigrid Juselius Foundation

Paivikki and Sakari Sohlberg Foundation

Finnish Foundation of Cardiovascular Research

Available from: 2017-12-22 Created: 2017-12-22 Last updated: 2018-02-16Bibliographically approved

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Oresic, Matej

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