Effects of chronic jet lag on the central and peripheral circadian clocks in CBA/N mice

Oct 24, 2013Chronobiology international

Chronic jet lag's effects on internal body clocks in the brain and organs of CBA/N mice

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Abstract

Chronic jet lag with 8-hour advances every 2 days over 10 days alters the phase of clock genes in CBA/N mice.

Chronic jet lag shifted the temporal expression of most clock genes in the suprachiasmatic nucleus without completely disrupting circadian rhythms.
In the liver, the expression of Per1, Bmal1, and Dbp was phase-shifted, while Per2 was significantly upregulated.
The chronic jet lag schedule significantly activated the expression of cell cycle-related genes c-Myc and p53 in the liver.
A positive correlation was observed between the expression of Per2 and p53.
Plasma levels of melatonin and corticosterone were not affected by chronic jet lag, suggesting stable overall hormonal levels.
Chronic jet lag suppressed the expression of MT1 melatonin and glucocorticoid receptors in the liver.

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The disruption of the circadian clock by frequent shifts in the light-dark cycle, such as shift-work or frequent jet lag, increases the risk of many diseases, including cancer. Experimental disruption of the circadian clock also increases tumor development in mice, although most studies used the strains that are genetically impaired in melatonin synthesis and secretion. Here, we examined the effects of experimental chronic jet lag with 8 h advances of the light-dark cycle every 2 days for 10 days on the central and peripheral clocks of CBA/N mice, the strain with normal profiles of melatonin synthesis and secretion. Mice were exposed to constant darkness after the 10 days of chronic jet lag. In the suprachiasmatic nucleus (SCN), chronic jet lag shifted the temporal expression of most clock genes examined without causing total disturbance of circadian oscillations. In the liver, the temporal patterns of Per1, Bmal1, and Dbp expression were phase-shifted, and Per2 expression was significantly upregulated by chronic jet lag. Further, the expression of cell cycle-related genes, c-Myc and p53 in the liver was significantly activated by the chronic jet lag schedule with a significant positive correlation between Per2 and p53 expression. We determined the plasma concentrations of melatonin and corticosterone as candidate hormonal messengers of chronic jet lag, but their overall levels were not affected by chronic jet lag. Moreover, the expression of the MT1 melatonin and glucocorticoid receptors in the liver was suppressed by chronic jet lag. These data suggest that in CBA/N mice, frequent advances of light-dark cycles modify the phases of central clock in the SCN and disturb the peripheral clock in the liver and apoptotic functions, which may be associated with the suppression of hormone receptors.

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Effects of chronic jet lag on the central and peripheral circadian clocks in CBA/N mice

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