Regulation of Circadian Gene Expression in Liver by Systemic Signals and Hepatocyte Oscillators

Kornmann, Benoı̂t; Schaad, Olivier; Reinke, Hans; Saini, Camille; Schibler, Ueli

doi:10.1101/sqb.2007.72.041

Cited by 94 publications

(84 citation statements)

References 48 publications

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“…We also demonstrated the functional disruption of the hepatocyte clock by describing the marked decrease in the number and amplitude of oscillating transcripts in the liver. This result is in line with that of a different mouse model of hepatocyte circadian disruption in which the hepatocyte clock is arrested by the overexpression of REV-ERB alpha, a repressor of BMAL1 (25). We propose that the small percentage of oscillating liver transcripts not disrupted by hepatocyte deletion of Bmal1 represent transcripts from other cell types in the liver where the albumin promoter is not active (e.g., endothelial, Kupffer, and stellate cells, among others) or represent transcripts that are entrained by the central clock through factors such as feeding or hormones.…”

Section: Discussionsupporting

confidence: 75%

Hepatocyte circadian clock controls acetaminophen bioactivation through NADPH-cytochrome P450 oxidoreductase

Johnson

Walisser

Liu

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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The diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) reportedly is driven by oscillations in metabolism that are influenced by the circadian phases of feeding and fasting. To determine the relative contributions of the central clock and the hepatocyte circadian clock in modulating the chronotoxicity of APAP, we used a conditional null allele of brain and muscle Arntlike 1 (Bmal1, aka Mop3 or Arntl) allowing deletion of the clock from hepatocytes while keeping the central and other peripheral clocks (e.g., the clocks controlling food intake) intact. We show that deletion of the hepatocyte clock dramatically reduces APAP bioactivation and toxicity in vivo and in vitro because of a reduction in NADPH-cytochrome P450 oxidoreductase gene expression, protein, and activity.circadian clock | acetaminophen toxicity | NADPH-cytochrome P450 oxidoreductase | chronotoxicity | Bmal1

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Section: Discussionsupporting

confidence: 75%

Hepatocyte circadian clock controls acetaminophen bioactivation through NADPH-cytochrome P450 oxidoreductase

Johnson

Walisser

Liu

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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“…When both zeitgebers (LD and feeding-fasting cycles) are present, the brain oscillators appear to be driven by the LD cycle, whereas the clock gene oscillations in the liver are more dependent on feeding schedule (zebrafish: López-Olmeda et al 2010;sea bream: Vera et al 2013). In goldfish, a unique meal may shift the clock gene rhythms in the liver (Feliciano et al 2011), which matches the findings in mammals, where a high dependence of clock liver entrainment on feeding cues has been reported (Stokkan et al 2001, Kornmann et al 2007, Patton & Mistlberger 2013. Exactly how feeding-fasting cycles entrain endogenous clocks remains unknown, but it is expected that hormones, metabolites or other energy sensor molecules that cycle with feeding status induce acute changes in clock gene expression that shift the clocks (Figs 1 and 2).…”

Section: :3supporting

confidence: 62%

Interplay between the endocrine and circadian systems in fishes

Isorna

Pedro

Valenciano

et al. 2017

Journal of Endocrinology

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The circadian system is responsible for the temporal organisation of physiological functions which, in part, involves daily cycles of hormonal activity. In this review, we analyse the interplay between the circadian and endocrine systems in fishes. We first describe the current model of fish circadian system organisation and the basis of the molecular clockwork that enables different tissues to act as internal pacemakers. This system consists of a net of central and peripherally located oscillators and can be synchronised by the light-darkness and feeding-fasting cycles. We then focus on two central neuroendocrine transducers (melatonin and orexin) and three peripheral hormones (leptin, ghrelin and cortisol), which are involved in the synchronisation of the circadian system in mammals and/or energy status signalling. We review the role of each of these as overt rhythms (i.e. outputs of the circadian system) and, for the first time, as key internal temporal messengers that act as inputs for other endogenous oscillators. Based on acute changes in clock gene expression, we describe the currently accepted model of endogenous oscillator entrainment by the light-darkness cycle and propose a new model for non-photic (endocrine) entrainment, highlighting the importance of the bidirectional cross-talking between the endocrine and circadian systems in fishes. The flexibility of the fish circadian system combined with the absence of a master clock makes these vertebrates a very attractive model for studying communication among oscillators to drive functionally coordinated outputs.

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“…By using this system in conjunction with genome-wide transcriptome profiling, they identified ;50 genes whose cyclic expression was driven by systemic cues supposedly emanating from the SCN rather than driven by local hepatocyte oscillators (Kornmann et al 2007b). The list of these genes contains Per2 and several genes whose expression is known to be modulated by temperature, such as Hsp genes and genes encoding cold-inducible RNA-binding proteins.…”

Section: Body Temperature Rhythms As Zeitgebers For Peripheral Circadmentioning

confidence: 99%

Simulated body temperature rhythms reveal the phase-shifting behavior and plasticity of mammalian circadian oscillators

Saini

Morf²,

Stratmann³

et al. 2012

Genes Dev.

226

189

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The circadian pacemaker in the suprachiasmatic nuclei (SCN) of the hypothalamus maintains phase coherence in peripheral cells through metabolic, neuronal, and humoral signaling pathways. Here, we investigated the role of daily body temperature fluctuations as possible systemic cues in the resetting of peripheral oscillators. Using precise temperature devices in conjunction with real-time monitoring of the bioluminescence produced by circadian luciferase reporter genes, we showed that simulated body temperature cycles of mice and even humans, with daily temperature differences of only 3°C and 1°C, respectively, could gradually synchronize circadian gene expression in cultured fibroblasts. The time required for establishing the new steady-state phase depended on the reporter gene, but after a few days, the expression of each gene oscillated with a precise phase relative to that of the temperature cycles. Smooth temperature oscillations with a very small amplitude could synchronize fibroblast clocks over a wide temperature range, and such temperature rhythms were also capable of entraining gene expression cycles to periods significantly longer or shorter than 24 h. As revealed by genetic loss-of-function experiments, heat-shock factor 1 (HSF1), but not HSF2, was required for the efficient synchronization of fibroblast oscillators to simulated body temperature cycles.[Keywords: circadian gene expression; body temperature rhythms; heat-shock factor 1 (HSF1); heat-shock factor 2 (HSF2)]

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Regulation of Circadian Gene Expression in Liver by Systemic Signals and Hepatocyte Oscillators

Cited by 94 publications

References 48 publications

Hepatocyte circadian clock controls acetaminophen bioactivation through NADPH-cytochrome P450 oxidoreductase

Hepatocyte circadian clock controls acetaminophen bioactivation through NADPH-cytochrome P450 oxidoreductase

Interplay between the endocrine and circadian systems in fishes

Simulated body temperature rhythms reveal the phase-shifting behavior and plasticity of mammalian circadian oscillators

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