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Gewählte Publikation:

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Publikationstyp: Zeitschriftenaufsatz
Dokumentart: Originalarbeit

Publikationsjahr: 2007

AutorInnen: Kuba, K; Zhang, L; Imai, Y; Arab, S; Chen, M; Maekawa, Y; Leschnik, M; Leibbrandt, A; Markovic, M; Makovic, M; Schwaighofer, J; Beetz, N; Musialek, R; Neely, GG; Komnenovic, V; Kolm, U; Metzler, B; Ricci, R; Hara, H; Meixner, A; Nghiem, M; Chen, X; Dawood, F; Wong, KM; Sarao, R; Cukerman, E; Kimura, A; Hein, L; Thalhammer, J; Liu, PP; Penninger, JM

Titel: Impaired heart contractility in Apelin gene-deficient mice associated with aging and pressure overload.

Quelle: Circ Res. 2007; 101(4):e32-e42



Autor/innen der Vetmeduni Vienna:

Kolm Ursula,
Leschnik Michael,
Markovic Mato,
Thalhammer Johann,

Beteiligte Vetmed-Organisationseinheiten
Klinische Abteilung für Interne Medizin Kleintiere,


Abstract:
Apelin constitutes a novel endogenous peptide system suggested to be involved in a broad range of physiological functions, including cardiovascular function, heart development, control of fluid homeostasis, and obesity. Apelin is also a catalytic substrate for angiotensin-converting enzyme 2, the key severe acute respiratory syndrome receptor. The in vivo physiological role of Apelin is still elusive. Here we report the generation of Apelin gene-targeted mice. Apelin mutant mice are viable and fertile, appear healthy, and exhibit normal body weight, water and food intake, heart rates, and heart morphology. Intriguingly, aged Apelin knockout mice developed progressive impairment of cardiac contractility associated with systolic dysfunction in the absence of histological abnormalities. We also report that pressure overload induces upregulation of Apelin expression in the heart. Importantly, in pressure overload-induced heart failure, loss of Apelin did not significantly affect the hypertrophy response, but Apelin mutant mice developed progressive heart failure. Global gene expression arrays and hierarchical clustering of differentially expressed genes in hearts of banded Apelin(-/y) and Apelin(+/y) mice showed concerted upregulation of genes involved in extracellular matrix remodeling and muscle contraction. These genetic data show that the endogenous peptide Apelin is crucial to maintain cardiac contractility in pressure overload and aging.

Keywords Pubmed: Aging/genetics
Aging/physiology*
Animals
Aorta
Blood Pressure/genetics
Blood Pressure/physiology*
Carrier Proteins/genetics*
Carrier Proteins/metabolism
Disease Models, Animal
Drinking Behavior
Echocardiography
Feeding Behavior
Female
Heart/embryology
Heart/physiology
Heart Failure/physiopathology*
Heart Failure/ultrasonography
Homeostasis/physiology
Intercellular Signaling Peptides and Proteins
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Myocardial Contraction/genetics
Myocardial Contraction/physiology*
Obesity/physiopathology
RNA, Messenger/metabolism
Severity of Illness Index


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