Author: Chen WD1, Wen MS1, Shie SS2, Lo YL3, Wo HT1, Wang CC1, Hsieh IC1, Lee TH4, Wang CY5.
Affiliation:
1Department of Cardiology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan. 2Department of Infectious Diseases, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan. 3Department of Thoracic Medicine, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan. 4Stroke Center and Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan. 5Department of Cardiology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taiwan. Electronic address: cwang@ocean.ag.
Conference/Journal: Biochem Biophys Res Commun.
Date published: 2014 Aug 7
Other:
Pages: S0006-291X(14)01401-6 , Special Notes: doi: 10.1016/j.bbrc.2014.07.138 , Word Count: 147
Circadian clocks are fundamental machinery in organisms ranging from archaea to humans. Disruption of the circadian system is associated with premature aging in mice, but the molecular basis underlying this phenomenon is still unclear. In this study, we found that telomerase activity exhibits endogenous circadian rhythmicity in humans and mice. Human and mouse TERT mRNA expression oscillates with circadian rhythms and are under the control of CLOCK-BMAL1 heterodimers. CLOCK deficiency in mice causes loss of rhythmic telomerase activities, TERT mRNA oscillation, and shortened telomere length. Physicians with regular work schedules have circadian oscillation of telomerase activity while emergency physicians working in shifts lose the circadian rhythms of telomerase activity. These findings identify the circadian rhythm as a mechanism underlying telomere and telomerase activity control that serve as interconnections between circadian systems and aging.
Copyright © 2014 Elsevier Inc. All rights reserved.
KEYWORDS:
Aging; Circadian rhythm; Telomerase activity; Telomere
PMID: 25109806