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Altitude, temperature, circadian rhythms and exercise
Published in Adam P. Sharples, James P. Morton, Henning Wackerhage, Molecular Exercise Physiology, 2022
Henning Wackerhage, Kenneth A. Dyar, Martin Schönfelder
On the other hand, day-night differences in high-intensity exercise capacity are linked to exercise-induced hypoxemia and a glycolytic gene programme driven by hypoxia-inducible factor 1α (HIF-1α) (86). Like CLOCK and BMAL1, HIF-1α is a helix-loop-helix (bHLH) PER-ARNT-SIM (PAS) domain-containing transcription factor that can bind to the same regulatory sites in the genome. Interestingly, HIF-1α shows a bidirectional relationship with the circadian clock (90, 91). CLOCK and BMAL1 can drive 24 h Hif1a expression, and HIF-1α can synergise with BMAL and drive expression of common circadian clock and HIF target genes, including Per2 and Cry1. Accordingly, hypoxia can phase-shift clocks in a tissue-dependent manner (92). In mouse skeletal muscles this was shown to occur by a time-of-day-dependent interaction between HIF-1α and clock transcription factors (93). Further studies are needed to fully elucidate these relationships, but this data collectively suggests that moderate reductions in oxygen levels during high-intensity training, or even training under hypoxic conditions may be a more potent zeitgeber than lower or more moderate exercise bouts.
Endocrine Functions of Brain Dopamine
Published in Nira Ben-Jonathan, Dopamine, 2020
A rise of DA preceded the rise in PER2, and the elimination of DA from the brain, or the blockade of one of its receptors, results in decreased PER2, which can be reversed by administration of DA agonists. It has been proposed that retinal circadian activity is divided into two phases: (1) a DA-independent phase at low light intensities, and (2) a DA-dependent phase at high light intensities. Both phases have an impact on signaling the night-day transitions to the SCN.
Neurobiology of Mood Disorders
Published in Dr. Ather Muneer, Mood Disorders, 2018
Another measure of cellular metabolism is the ratio of AMP and ATP. An important sensor of the AMP/ATP ratio is adenosine monophosphate-dependent protein kinase (AMPK) which is activated upon binding to AMP. AMPK is stimulated in neurons in response to metabolic or ischemic stressors and elicits compensatory responses. AMPK phosphorylates casein kinase 1 epsilon which enhances phosphorylation of PER2, again directly pairing cellular metabolism to the circadian system.40 Moreover, the mitochondrial biogenesis stimulator, “peroxisome proliferator-activated receptor gamma coactivator 1-α”, directly regulates expression of BMAL1 and Rev-erbα and is necessary for circadian pacemaker function.41 The eventual results of metabolic dysfunction in neurons are oxidative stress, generation of reactive oxygen species and apoptosis. Therefore, given the close link between the circadian system and redox signaling, it seems reasonable to speculate that circadian rhythm disruption might lead to the accumulation of damaging free radicals and enhanced neuronal apoptosis. In fact the apoptotic genes, Wnt10, β-catenin, Dishevelled2 and transcription factor 3 promoters, are all bound by BMAL1, and Wnt pathway signaling is attenuated when BMAL1 levels are reduced. Aberrant Wnt and GSK3 signaling is implicated in mood disorders and there is emerging evidence to demonstrate that the circadian system is intimately involved in the regulation of these pathways.42
Pers reverse angiotensin II -induced vascular smooth muscle cell proliferation by targeting cyclin E expression via inhibition of the MAPK signaling pathway
Published in Chronobiology International, 2023
Wan Jin, Yu Tian, Yanyun Ding, Deixi Zhou, Long Li, Meng Yuan, Yuanzhu Wu, Mingqi Ye, Jiajie Luan, Kui Yang
Although we observed similar regulatory trends of Per1 and Per2 after Ang II stimulation, as well as a phase shift between mRNA and protein expression, there were slight differences in the time-dependent regulation of Per1 and Per2 at specific time points. We propose two possible reasons for these results. Firstly, existing literature has demonstrated that the timing of peak and trough in the periodic oscillations of Pers gene expression in in vitro experiments is time-dependent, with a constant anti-phase difference between limbs. The exact timing of phase and oscillations of the core clock, and their correlation with functional output oscillations, may vary from cell to cell, tissue to tissue, and from in vitro to in vivo. Secondly, Per1 and Per2 may play distinct roles in circadian oscillation. Ogawa et al. suggested that Per1 is part of a morning oscillator tracking dawn, while Per2 is part of an evening oscillator tracking dusk (Steinlechner et al. 2002). Furthermore, Riddle et al. demonstrated differential localization between Per1 and Per2 in the brain’s master circadian clock. The central SCN exhibited the highest abundance of PER1 protein, while higher expression of PER2 protein was observed in the rostral, dorsal, and caudal aspects compared to PER1 (Riddle et al. 2017). Therefore, the differences in PER1 and PER2 expression at certain time points may arise from variations in their functions and structures.
Recent advances in modulators of circadian rhythms: an update and perspective
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2020
Shenzhen Huang, Xinwei Jiao, Dingli Lu, Xiaoting Pei, Di Qi, Zhijie Li
Sleep plays a very important role in the biological process of all creatures; it is regulated by circadian rhythm and homeostatic mechanisms150. Normal circadian rhythms play an irreplaceable role in sleep. Circadian misalignments such as jet lag, shift work, and sleep deprivation have resulted in sleep disorders134,135. Kiessling’s group and Yamaguchi’s group identified that the different organs of mice showed heterogeneity entrainment kinetics in an experimental paradigm for jet lag151,152. The rhythm gene has been linked to sleep disorders. Mutations in both PER2 (PER2 S662G) and CSNK1D (CK1δ T44A) have been involved in familial advanced sleep phase syndrome (FASPS)153. Recent studies indicate that the core clock gene expression has a close association with sleep apnoea (SA). Canales et al.154 identified that the Per3 expression of SA was lower than that in the normal group. Pharmacological treatment targeting the mammalian clock has been shown to have beneficial effects on sleep architecture78. Compound 16 as an agonist of REV-ERBα and REV-ERBβ displays increase in wakefulness and reduction of paradoxical sleep-rapid eye movement (REM) sleep and slow-wave sleep in vivo67,78. Therefore, the REV-ERB ligands may be beneficial in treating sleep disorders.
Correlation among clock gene expression rhythms, sleep quality, and meal conditions in delayed sleep-wake phase disorder and night eating syndrome
Published in Chronobiology International, 2019
Atsushi Haraguchi, Yoko Komada, Yuichi Inoue, Shigenobu Shibata
The circadian clock system is common to almost all animals and plants, including humans, and in animals maintains various physiological functions, such as mood, body temperature, feeding pattern, and sleep-wake cycle, in an approximately 24-h rhythm (Mohawk et al., 2012). The circadian clock system is controlled by several clock genes, such as Cryptochrome1/2 (Cry1/2), Period1/2 (Per1/2), Brain and muscle arnt-like protein 1 (Bmal1), and Circadian locomotor output cycles kaput (Clock). These genes constitute a transcriptional-translational feedback loop that generates an approximately 24-h rhythm (Reppert and Weaver 2002). Mammals, including humans, have a central clock located in the suprachiasmatic nucleus (SCN) in the hypothalamus (Moore and Eichler 1972), and peripheral clocks located in peripheral organs and brain regions outside the SCN (Mohawk et al., 2012). Many studies indicate that mutations of clock genes can lead to disturbed circadian rhythms. For example, Per1/2 and Clock mutant mice show arrhythmical behavior under constant dark and 12-h-light/12-h-dark conditions, respectively (Turek et al., 2005; Zheng et al., 2001). Other studies in humans show that either Cry1/2 or Per2 mutations are associated with familial advanced sleep phase (FASP) (Hirano et al., 2016; Jones et al., 1999). These findings suggest that clock genes are important factors for maintaining physiological rhythms.