Cardiac hypertrophy, low blood pressure, and low aldosterone levels in mice devoid of the three circadian PAR bZip transcription factors DBP, HLF, and TEF.

Détails

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Etat: Public
Version: de l'auteur⸱e
ID Serval
serval:BIB_E62BDCCFF932
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Cardiac hypertrophy, low blood pressure, and low aldosterone levels in mice devoid of the three circadian PAR bZip transcription factors DBP, HLF, and TEF.
Périodique
American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Auteur⸱e⸱s
Wang Q., Maillard M., Schibler U., Burnier M., Gachon F.
ISSN
1522-1490[electronic], 0363-6119[linking]
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
299
Numéro
4
Pages
R1013-R1019
Langue
anglais
Résumé
The cardiovascular system is under the control of the circadian clock, and disturbed circadian rhythms can induce cardiovascular pathologies. This cyclic regulation is probably brought about by the circadian expression of genes encoding enzymes and regulators involved in cardiovascular functions. We have previously shown that the rhythmic transcription of output genes is, in part, regulated by the clock-controlled PAR bZip transcription factors DBP (albumin D-element Binding Protein), HLF (Hepatic Leukemia Factor), and TEF (Thyrotroph Embryonic Factor). The simultaneous deletion of all three PAR bZip transcription factors leads to increased morbidity and shortened life span. Here, we demonstrate that Dbp/Tef/Hlf triple knockout mice develop cardiac hypertrophy and left ventricular dysfunction associated with a low blood pressure. These dysfunctions are exacerbated by an abnormal response to this low blood pressure characterized by low aldosterone levels. The phenotype of PAR bZip knockout mice highlights the importance of circadian regulators in the modulation of cardiovascular functions.
Mots-clé
circadian clock, PAR bZip transcription factors, cardiac physiology, blood pressure, kidney function
Pubmed
Web of science
Création de la notice
30/07/2010 17:30
Dernière modification de la notice
20/10/2020 15:41
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