scholarly journals Chronic Treatment with Prednisolone Represses the Circadian Oscillation of Clock Gene Expression in Mouse Peripheral Tissues

2006 ◽  
Vol 20 (3) ◽  
pp. 573-583 ◽  
Author(s):  
Satoru Koyanagi ◽  
Sumako Okazawa ◽  
Yukako Kuramoto ◽  
Kentarou Ushijima ◽  
Hiroshi Shimeno ◽  
...  
2018 ◽  
Vol Volume 10 ◽  
pp. 203-215 ◽  
Author(s):  
Daniela Meneses-Santos ◽  
Daniella do Carmo Buonfiglio ◽  
Rodrigo Antonio Peliciari-Garcia ◽  
Angela Maria Ramos-Lobo ◽  
Divanízia do Nascimento Souza ◽  
...  

Endocrinology ◽  
2016 ◽  
Vol 157 (4) ◽  
pp. 1522-1534 ◽  
Author(s):  
Elizabeth R. Woodruff ◽  
Lauren E. Chun ◽  
Laura R. Hinds ◽  
Robert L. Spencer

Abstract Mood disorders are associated with dysregulation of prefrontal cortex (PFC) function, circadian rhythms, and diurnal glucocorticoid (corticosterone [CORT]) circulation. Entrainment of clock gene expression in some peripheral tissues depends on CORT. In this study, we characterized over the course of the day the mRNA expression pattern of the core clock genes Per1, Per2, and Bmal1 in the male rat PFC and suprachiasmatic nucleus (SCN) under different diurnal CORT conditions. In experiment 1, rats were left adrenal-intact (sham) or were adrenalectomized (ADX) followed by 10 daily antiphasic (opposite time of day of the endogenous CORT peak) ip injections of either vehicle or 2.5 mg/kg CORT. In experiment 2, all rats received ADX surgery followed by 13 daily injections of vehicle or CORT either antiphasic or in-phase with the endogenous CORT peak. In sham rats clock gene mRNA levels displayed a diurnal pattern of expression in the PFC and the SCN, but the phase differed between the 2 structures. ADX substantially altered clock gene expression patterns in the PFC. This alteration was normalized by in-phase CORT treatment, whereas antiphasic CORT treatment appears to have eliminated a diurnal pattern (Per1 and Bmal1) or dampened/inverted its phase (Per2). There was very little effect of CORT condition on clock gene expression in the SCN. These experiments suggest that an important component of glucocorticoid circadian physiology entails CORT regulation of the molecular clock in the PFC. Consequently, they also point to a possible mechanism that contributes to PFC disrupted function in disorders associated with abnormal CORT circulation.


2007 ◽  
Vol 293 (4) ◽  
pp. R1528-R1537 ◽  
Author(s):  
David J. Kennaway ◽  
Julie A. Owens ◽  
Athena Voultsios ◽  
Michael J. Boden ◽  
Tamara J. Varcoe

The role of peripheral vs. central circadian rhythms and Clock in the maintenance of metabolic homeostasis and with aging was examined by using ClockΔ19 +MEL mice. These have preserved suprachiasmatic nucleus and pineal gland rhythmicity but arrhythmic Clock gene expression in the liver and skeletal muscle. ClockΔ19 +MEL mice showed fasting hypoglycemia in young-adult males, fasting hyperglycemia in older females, and substantially impaired glucose tolerance overall. ClockΔ19 +MEL mice had substantially reduced plasma insulin and plasma insulin/glucose nocturnally in males and during a glucose tolerance test in females, suggesting impaired insulin secretion. ClockΔ19 +MEL mice had reduced hepatic expression and loss of rhythmicity of gck, pfkfb3, and pepck mRNA, which is likely to impair glycolysis and gluconeogenesis. ClockΔ19 +MEL mice also had reduced glut4 mRNA in skeletal muscle, and this may contribute to poor glucose tolerance. Whole body insulin tolerance was enhanced in ClockΔ19 +MEL mice, however, suggesting enhanced insulin sensitivity. These responses occurred although the ClockΔ19 mutation did not cause obesity and reduced plasma free fatty acids while increasing plasma adiponectin. These studies on clock-gene disruption in peripheral tissues and metabolic homeostasis provide compelling evidence of a relationship between circadian rhythms and the glucose/insulin and adipoinsular axes. It is, however, premature to declare that clock-gene disruption causes the full metabolic syndrome.


2007 ◽  
Vol 26 (10) ◽  
pp. 2731-2738 ◽  
Author(s):  
Mitsugu Sujino ◽  
Mamoru Nagano ◽  
Atsuko Fujioka ◽  
Yasufumi Shigeyoshi ◽  
Shin-Ichi T. Inouye

2021 ◽  
pp. jeb.233213
Author(s):  
Grace H. Goh ◽  
Dominique Blache ◽  
Peter J. Mark ◽  
W. Jason Kennington ◽  
Shane K. Maloney

Circadian rhythms optimize health by coordinating the timing of physiological processes to match predictable daily environmental challenges. The circadian rhythm of body temperature is thought to be an important modulator of molecular clocks in peripheral tissues, but how daily temperature cycles impact physiological function is unclear. Here, we examined the effect of constant (25°C, TCON) and cycling (28°C/22°C during light/dark, TCYC) temperature paradigms on lifespan of Drosophila melanogaster, and the expression of clock genes, Heat shock protein 83 (Hsp83), Frost (Fst), and Senescence-associated protein 30 (smp-30). Male and female Drosophila housed at TCYC had longer median lifespans than those housed at TCON. TCYC induced robust Hsp83 rhythms and rescued the age-related decrease in smp-30 expression that was observed in flies at TCON, potentially indicating an increased capacity to cope with age-related cellular stress. Ageing under TCON led to a decrease in the amplitude of expression of all clock genes in the bodies of male flies, except for cyc, which was non-rhythmic, and for per and cry in female flies. Strikingly, housing under TCYC conditions rescued the age-related decrease in amplitude of all clock genes, and generated rhythmicity in cyc expression, in the male flies, but not the female flies. The results suggest that ambient temperature rhythms modulate Drosophila lifespan, and that the amplitude of clock gene expression in peripheral body clocks may be a potential link between temperature rhythms and longevity in male Drosophila. Longevity due to TCYC appeared predominantly independent of clock gene amplitude in female Drosophila.


2017 ◽  
Vol 28 (17) ◽  
pp. 2333-2342 ◽  
Author(s):  
Isao T. Tokuda ◽  
Akihiko Okamoto ◽  
Ritsuko Matsumura ◽  
Toru Takumi ◽  
Makoto Akashi

Limit-cycle oscillations require the presence of nonlinear processes. Although mathematical studies have long suggested that multiple nonlinear processes are required for autonomous circadian oscillation in clock gene expression, the underlying mechanism remains controversial. Here we show experimentally that cell-autonomous circadian transcription of a mammalian clock gene requires a functionally interdependent tandem E-box motif; the lack of either of the two E-boxes results in arrhythmic transcription. Although previous studies indicated the role of the tandem motifs in increasing circadian amplitude, enhancing amplitude does not explain the mechanism for limit-cycle oscillations in transcription. In this study, mathematical analysis suggests that the interdependent behavior of enhancer elements including not only E-boxes but also ROR response elements might contribute to limit-cycle oscillations by increasing transcriptional nonlinearity. As expected, introduction of the interdependence of circadian enhancer elements into mathematical models resulted in autonomous transcriptional oscillation with low Hill coefficients. Together these findings suggest that interdependent tandem enhancer motifs on multiple clock genes might cooperatively enhance nonlinearity in the whole circadian feedback system, which would lead to limit-cycle oscillations in clock gene expression.


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