Circadian Clock-Deficient Mice as a Tool for Exploring Disease Etiology

Doi, Masao

doi:10.1248/bpb.b12-00364

Cited by 29 publications

(25 citation statements)

References 65 publications

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“…Significant disturbance of the 24 h sleep/wake rhythm, whether or not the consequence of a sleep disorder, that typically occurs with bedroom ALAN exposure induces modification of the A and/or Φ of the core body temperature circadian rhythm that in turn alters the A and/or Φ of the central plasma blood volume, melatonin and autonomic nervous system circadian rhythms. Furthermore, aging, renal disease, metabolic disorders and salt sensitivity commonly give rise to perturbation of the A, mean level and sometimes Φ of the renal H 2 O and Na + handling circadian rhythms in association with CD of the RAAS, ANP, AVP and calcitonin gene-related peptide systems (Asplund, 1995;Boer-Martins et al, 2011;Bonny & Firsov, 2013;Doi, 2012;Ishigaki, 2016;Isobe et al, 2015;Natsume, 2006;Ouslander et al, 1998;Portaluppi et al, 1992;Smolensky et al, 2016;Trasforini et al, 1991). Such CTS alterations favor sleep-time nondipping and rising BP 24 h patterns -nocturnal hypertension (Smolensky et al, 2016).…”

Section: Non-dipper and Riser Bp 24 H Patterning (Sleeptime Hypertensmentioning

confidence: 99%

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

147

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Biological processes are organized in time as innate rhythms defined by the period (τ), phase (peak [Φ] and trough time), amplitude (A, peak-trough difference) and mean level. The human time structure in its entirety is comprised of ultradian (τ < 20 h), circadian (20 h > τ < 28 h) and infradian (τ > 28 h) bioperiodicities. The circadian time structure (CTS) of human beings, which is more complicated than in lower animals, is orchestrated and staged by a brain central multioscillator system that includes a prominent pacemaker - the suprachiasmatic nuclei of the hypothalamus. Additional pacemaker activities are provided by the pineal hormone melatonin, which circulates during the nighttime, and the left and right cerebral cortices. Under ordinary circumstances this system coordinates the τ and Φ of rhythms driven by subservient peripheral cell, tissue and organ clock networks. Cyclic environmental, feeding and social time cues synchronize the endogenous 24 h clocks and rhythms. Accordingly, processes and functions of the internal environment are integrated in time for maximum biological efficiency, and they are also organized and synchronized in time to the external environment to ensure optimal performance and response to challenge. Artificial light at night (ALAN) exposure can alter the CTS as can night work, which, like rapid transmeridian displacement by air travel, necessitates realignment of the Φ of the multitude of 24 h rhythms. In 2001, Stevens and Rea coined the phrase "circadian disruption" (CD) to label the CTS misalignment induced by ALAN and shift work (SW) as a potential pathologic mechanism of the increased risk for cancer and other medical conditions. Current concerns relating to the effects of ALAN exposure on the CTS motivated us to renew our long-standing interest in the possible role of CD in the etiopathology of common human diseases and patient care. A surprisingly large number of medical conditions involve CD: adrenal insufficiency; nocturia; sleep-time non-dipping and rising blood pressure 24 h patterns (nocturnal hypertension); delayed sleep phase syndrome, non-24 h sleep/wake disorder; recurrent hypersomnia; SW intolerance; delirium; peptic ulcer disease; kidney failure; depression; mania; bipolar disorder; Parkinson's disease; Smith-Magenis syndrome; fatal familial insomnia syndrome; autism spectrum disorder; asthma; byssinosis; cancers; hand, foot and mouth disease; post-operative state; and ICU outcome. Poorly conceived medical interventions, for example nighttime dosing of synthetic corticosteroids and certain β-antagonists and cyclic nocturnal enteral or parenteral nutrition, plus lifestyle habits, including atypical eating times and chronic alcohol consumption, also can be causal of CD. Just as surprisingly are the many proven chronotherapeutic strategies available today to manage the CD of several of these medical conditions. In clinical medicine, CD seems to be a common, yet mostly unrecognized, pathologic mechanism of human disease as are the many effective chronotherapeutic int...

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Section: Non-dipper and Riser Bp 24 H Patterning (Sleeptime Hypertensmentioning

confidence: 99%

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Smolensky

Hermida

Reinberg

et al. 2016

Chronobiology International

147

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“…In contrast, Bmal1 knockout mice are hypotensive (Curtis et al, 2007). Importantly, this enzyme is functionally conserved in humans, and the pathophysiology of human idiopathic hyperaldosteronism resembles that of Cry1/2-deficient mice (reviewed in Doi, 2012;Ota et al, 2012). Importantly, this enzyme is functionally conserved in humans, and the pathophysiology of human idiopathic hyperaldosteronism resembles that of Cry1/2-deficient mice (reviewed in Doi, 2012;Ota et al, 2012).…”

Section: (B) Circadian Regulation Of Gc Action Prior To Binding To Gmentioning

confidence: 99%

Adrenal Clocks and the Role of Adrenal Hormones in the Regulation of Circadian Physiology

et al. 2014

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The mammalian circadian timing system consists of a master pacemaker in the suprachiasmatic nucleus (SCN) and subordinate clocks that disseminate time information to various central and peripheral tissues. While the function of the SCN in circadian rhythm regulation has been extensively studied, we still have limited understanding of how peripheral tissue clock function contributes to the regulation of physiological processes. The adrenal gland plays a special role in this context as adrenal hormones show strong circadian secretion rhythms affecting downstream physiological processes. At the same time, they have been shown to affect clock gene expression in various other tissues, thus mediating systemic entrainment to external zeitgebers and promoting internal circadian alignment. In this review, we discuss the function of circadian clocks in the adrenal gland, how they are reset by the SCN and may further relay time-of-day information to other tissues. Focusing on glucocorticoids, we conclude by outlining the impact of adrenal rhythm disruption on neuropsychiatric, metabolic, immune, and malignant disorders.

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“…However, this canonical view was recently revised due to the observation that the alternative isoform, HSD3B1, is expressed within zona glomerulosa (ZG) cells (5,6), where aldosterone is produced. Interestingly, the mouse also has two isoforms in the adrenal: one (Hsd3b1) is ubiquitous in the cortex, but the other (Hsd3b6) is ZG specific (6)(7)(8)(9). Thus, in both species, the adrenals possess a ZG-specific isoform, in addition to the ubiquitous one.…”

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confidence: 99%

Angiotensin II Triggers Expression of the Adrenal Gland Zona Glomerulosa-Specific 3β-Hydroxysteroid Dehydrogenase Isoenzyme through De Novo Protein Synthesis of the Orphan Nuclear Receptors NGFIB and NURR1

Ota

Doi

Yamazaki

et al. 2014

Molecular and Cellular Biology

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The 3␤-hydroxysteroid dehydrogenase (3␤-HSD) is an enzyme crucial for steroid synthesis. Two different 3␤-HSD isoforms exist in humans. Classically, HSD3B2 was considered the principal isoform present in the adrenal. However, we recently showed that the alternative isoform, HSD3B1, is expressed specifically within the adrenal zona glomerulosa (ZG), where aldosterone is produced, raising the question of why this isozyme needs to be expressed in this cell type. Here we show that in both human and mouse, expression of the ZG isoform 3␤-HSD is rapidly induced upon angiotensin II (AngII) stimulation. AngII is the key peptide hormone regulating the capacity of aldosterone synthesis. Using the human adrenocortical H295R cells as a model system, we show that the ZG isoform HSD3B1 differs from HSD3B2 in the ability to respond to AngII. Mechanistically, the induction of HSD3B1 involves de novo protein synthesis of the nuclear orphan receptors NGFIB and NURR1. The HSD3B1 promoter contains a functional NGFIB/NURR1-responsive element to which these proteins bind in response to AngII. Knockdown of these proteins and overexpression of a dominant negative NGFIB both reduce the AngII responsiveness of HSD3B1. Thus, the AngII-NGFIB/NURR1 pathway controls HSD3B1. Our work reveals HSD3B1 as a new regulatory target of AngII.T he enzyme 3␤-hydroxysteroid dehydrogenase/⌬ 5 -⌬ 4 -isomerase (3␤-HSD) is essential for the biosynthesis of all active steroid hormones, including those secreted from the adrenal gland (1-4). Whereas two distinct 3␤-HSD isoforms (type I 3␤-HSD, which is encoded by HSD3B1, and type II 3␤-HSD, which is encoded by HSD3B2) exist in humans, it has long been thought that type II 3␤-HSD was the only isoform expressed in the human adrenal glands (1). However, this canonical view was recently revised due to the observation that the alternative isoform, HSD3B1, is expressed within zona glomerulosa (ZG) cells (5, 6), where aldosterone is produced. Interestingly, the mouse also has two isoforms in the adrenal: one (Hsd3b1) is ubiquitous in the cortex, but the other (Hsd3b6) is ZG specific (6-9). Thus, in both species, the adrenals possess a ZG-specific isoform, in addition to the ubiquitous one. However, it remains unknown why these different enzymes are expressed simultaneously in ZG cells. Since these isozymes catalyze the same enzymatic reaction, the question remains open why the newly identified ZG-specific isoform needs to be expressed in ZG cells.Angiotensin II (AngII) is the key peptide hormone in the renin-angiotensin-aldosterone system (RAAS). AngII is a potent secretagogue of the mineralocorticoid aldosterone, which is principally synthesized within the adrenal gland ZG cells through a series of enzymatic reactions that involve multiple enzymes, including 3␤-HSDs. The actions of AngII on ZG cells are often divided into two temporally different phases (10-12): (i) an early (within minutes after stimulation) upregulation of aldosterone synthesis through posttranslational activation of steroidogenic acute regulatory...

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Circadian Clock-Deficient Mice as a Tool for Exploring Disease Etiology

Cited by 29 publications

References 65 publications

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Circadian disruption: New clinical perspective of disease pathology and basis for chronotherapeutic intervention

Adrenal Clocks and the Role of Adrenal Hormones in the Regulation of Circadian Physiology

Angiotensin II Triggers Expression of the Adrenal Gland Zona Glomerulosa-Specific 3β-Hydroxysteroid Dehydrogenase Isoenzyme through De Novo Protein Synthesis of the Orphan Nuclear Receptors NGFIB and NURR1

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