scholarly journals Different Effects of Phase Advance and Delay in Rotating Light-Dark Regimens on Clock and Natriuretic Peptide Gene Expression in the Rat Heart

2014 ◽  
pp. S573-S584 ◽  
Author(s):  
I. HERICHOVÁ ◽  
J. AMBRUŠOVÁ ◽  
Ľ. MOLČAN ◽  
A. VESELÁ ◽  
P. SVITOK ◽  
...  
Keyword(s):  
Gene Expression ◽  
Clock Genes ◽  
Active Phase ◽  
Circadian System ◽  
Daily Rhythm ◽  
Male Rats ◽  
Phase Advance ◽  
Peripheral Oscillators ◽  
Peptide Gene ◽  
Central Oscillator

Under physiological conditions the mammalian circadian system is synchronized to a cyclic environment. The central oscillator in the suprachiasmatic nuclei (SCN) responds predominantly to an external light (L) dark (D) cycle. Peripheral oscillators are more efficiently synchronized by metabolic cues. When the circadian system is exposed to opposing synchronizing cues, peripheral oscillators uncouple from the SCN. To consider influence of phase advances and delays in light regimens mimicking shift work, we analyzed the expression of clock genes (per2, bmal1) and natriuretic peptides (anp, bnp) in the heart of male rats. Experimental groups were exposed to a rotating LD regimen with either 8 h phase advance or delay for 11 weeks. Samples were taken for a 24 h cycle in 4 h intervals. Peripheral oscillators responded to rotating phase advance by decreasing rhythm robustness, while phase delay mostly influenced the phase angle between the acrophase of rhythmic gene expression and the external LD cycle. The expression of anp was arrhythmic in the heart of control rats and was not influenced by rotating LD regimens. The expression of bnp showed a daily rhythm with a nadir during the active phase. The daily rhythm in bnp expression diminished under rotating LD regimen conditions.

scholarly journals Daily rhythms in gene expression of the human parasite Schistosoma mansoni

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Kate A. Rawlinson ◽  
Adam J. Reid ◽  
Zhigang Lu ◽  
Patrick Driguez ◽  
Anna Wawer ◽  
...  
Keyword(s):  
Gene Expression ◽  
Schistosoma Mansoni ◽  
Circadian Clock ◽  
Drug Targets ◽  
Clock Genes ◽  
Biological Rhythms ◽  
Active Phase ◽  
Egg Laying ◽  
Daily Rhythms ◽  
Metazoan Parasites

Abstract Background The consequences of the earth’s daily rotation have led to 24-h biological rhythms in most organisms. Even some parasites are known to have daily rhythms, which, when in synchrony with host rhythms, can optimise their fitness. Understanding these rhythms may enable the development of control strategies that take advantage of rhythmic vulnerabilities. Recent work on protozoan parasites has revealed 24-h rhythms in gene expression, drug sensitivity and the presence of an intrinsic circadian clock; however, similar studies on metazoan parasites are lacking. To address this, we investigated if a metazoan parasite has daily molecular oscillations, whether they reveal how these longer-lived organisms can survive host daily cycles over a lifespan of many years and if animal circadian clock genes are present and rhythmic. We addressed these questions using the human blood fluke Schistosoma mansoni that lives in the vasculature for decades and causes the tropical disease schistosomiasis. Results Using round-the-clock transcriptomics of male and female adult worms collected from experimentally infected mice, we discovered that ~ 2% of its genes followed a daily pattern of expression. Rhythmic processes included a stress response during the host’s active phase and a ‘peak in metabolic activity’ during the host’s resting phase. Transcriptional profiles in the female reproductive system were mirrored by daily patterns in egg laying (eggs are the main drivers of the host pathology). Genes cycling with the highest amplitudes include predicted drug targets and a vaccine candidate. These 24-h rhythms may be driven by host rhythms and/or generated by a circadian clock; however, orthologs of core clock genes are missing and secondary clock genes show no 24-h rhythmicity. Conclusions There are daily rhythms in the transcriptomes of adult S. mansoni, but they appear less pronounced than in other organisms. The rhythms reveal temporally compartmentalised internal processes and host interactions relevant to within-host survival and between-host transmission. Our findings suggest that if these daily rhythms are generated by an intrinsic circadian clock then the oscillatory mechanism must be distinct from that in other animals. We have shown which transcripts oscillate at this temporal scale and this will benefit the development and delivery of treatments against schistosomiasis.

Dormancy, Diapause, and the Role of the Circadian System in Insect Photoperiodism

2020 ◽  
Vol 65 (1) ◽  
pp. 373-389 ◽  
Author(s):  
David S. Saunders
Keyword(s):  
Clock Genes ◽  
Animal Experiments ◽  
Transcript Abundance ◽  
Circadian System ◽  
Gene Transcript ◽  
Light Cycle ◽  
Peripheral Oscillators ◽  
Circadian Clock Genes ◽  
Similar Phase

Whole-animal experiments devised to investigate possible association between photoperiodic time measurement and the circadian system (Bünning's hypothesis) are compared with more recent molecular investigations of circadian clock genes. In Sarcophaga argyrostoma and some other species, experimental cycles of light and darkness revealed a photoperiodic oscillator, set to constant phase at dusk and measuring night length repeatedly during extended periods of darkness. In some species, however, extreme dampening revealed an unrepetitive (i.e., hourglass-like) response. Rhythms of clock gene transcript abundance may also show similar phase relationships to the light cycle, and gene silencing of important clock genes indicates that they play a crucial role in photoperiodism either alone or in concert. However, the multiplicity of peripheral oscillators in the insect circadian system indicates that more complex mechanisms might also be important.

Rhythmic Release of Corticosterone Induces Circadian Clock Gene Expression in the Cerebellum

2019 ◽  
Vol 110 (7-8) ◽  
pp. 604-615 ◽  
Author(s):  
Tenna Bering ◽  
Henrik Hertz ◽  
Martin Fredensborg Rath
Keyword(s):  
Gene Expression ◽  
In Situ Hybridization ◽  
Glucocorticoid Receptor ◽  
Cerebellar Cortex ◽  
Clock Gene ◽  
Clock Genes ◽  
Circadian Oscillator ◽  
Male Rats ◽  
Clock Gene Expression

Neurons of the cerebellar cortex contain a circadian oscillator, with circadian expression of clock genes being controlled by the master clock of the suprachiasmatic nucleus (SCN). However, the signaling pathway connecting the SCN to the cerebellum is unknown. Glucocorticoids exhibit a prominent SCN-dependent circadian rhythm, and high levels of the glucocorticoid receptor have been reported in the cerebellar cortex; we therefore hypothesized that glucocorticoids may control the rhythmic expression of clock genes in the cerebellar cortex. We here applied a novel methodology by combining the electrolytic lesion of the SCN with implantation of a micropump programmed to release corticosterone in a circadian manner mimicking the endogenous hormone profile. By use of this approach, we were able to restore the corticosterone rhythm in SCN-lesioned male rats. Clock gene expression in the cerebellum was abolished in rats with a lesioned SCN, but exogenous corticosterone restored the daily rhythm in clock gene expression in the cerebellar cortex, as revealed by quantitative real-time PCR and radiochemical in situ hybridization for the detection of the core clock genes Per1, Per2, and Arntl. On the contrary, exogenous hormone did not restore circadian rhythms in body temperature and running activity. RNAscope in situ hybridization further revealed that the glucocorticoid receptor colocalizes with clock gene products in cells of the cerebellar cortex, suggesting that corticosterone exerts its actions by binding directly to receptors in neurons of the cerebellum. However, rhythmic clock gene expression in the cerebellum was also detectable in adrenalectomized rats, indicating that additional control mechanisms exist. These data show that the cerebellar circadian oscillator is influenced by SCN-dependent rhythmic release of corticosterone.

scholarly journals Regulation of Melanopsins andPer1byα-MSH and Melatonin in PhotosensitiveXenopus laevisMelanophores

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Maria Nathália de Carvalho Magalhães Moraes ◽  
Luciane Rogéria dos Santos ◽  
Nathana Mezzalira ◽  
Maristela Oliveira Poletini ◽  
Ana Maria de Lauro Castrucci
Keyword(s):  
Gene Expression ◽  
Circadian Rhythms ◽  
Intracellular Signaling ◽  
Cultured Cells ◽  
Clock Genes ◽  
Circadian System ◽  
Time Of Application ◽  
Intracellular Signaling Pathways ◽  
Peripheral Clocks ◽  
Internal Signal

α-MSH and light exert a dispersing effect on pigment granules ofXenopus laevismelanophores; however, the intracellular signaling pathways are different. Melatonin, a hormone that functions as an internal signal of darkness for the organism, has opposite effects, aggregating the melanin granules. Because light functions as an important synchronizing signal for circadian rhythms, we further investigated the effects of both hormones on genes related to the circadian system, namely,Per1(one of the clock genes) and the melanopsins,Opn4xandOpn4m(photopigments).Per1showed temporal oscillations, regardless of the presence of melatonin orα-MSH, which slightly inhibited its expression. Melatonin effects on melanopsins depend on the time of application: if applied in the photophase it dramatically decreasedOpn4xandOpn4mexpressions, and abolished their temporal oscillations, opposite toα-MSH, which increased the melanopsins’ expressions. Our results demonstrate that unlike what has been reported for other peripheral clocks and cultured cells, medium changes or hormones do not play a major role in synchronizing theXenopusmelanophore population. This difference is probably due to the fact thatX. laevismelanophores possess functional photopigments (melanopsins) that enable these cells to primarily respond to light, which triggers melanin dispersion and modulates gene expression.

Synchronization of Fibroblasts Ex Vivo in Psychopharmacology

2020 ◽  
Author(s):  
Frank Faltraco ◽  
Adriana Uzoni ◽  
Liliia Shevchuk ◽  
Johannes Thome ◽  
Denise Palm
Keyword(s):  
Current Knowledge ◽  
Ex Vivo ◽  
Circadian System ◽  
Suprachiasmatic Nuclei ◽  
Circadian Gene ◽  
Peripheral Oscillators ◽  
Rat Fibroblasts ◽  
Inner Clock ◽  
Central Oscillator

AbstractThe central oscillator for the inner clock is the suprachiasmatic nuclei of the hypothalamus. Furthermore, many peripheral oscillators are present in tissues such as skin. Human derived fibroblasts provide an advantageous model to study circadian rhythmicity as well as the influence of pharmacological drugs on circadian gene expression. Importantly, the synchronization of the circadian system of fibroblasts can be done by different methods. The review presents an overview of the current knowledge of different synchronization methods mostly used in mice or rat fibroblasts. Furthermore, the review sums up and discusses the role of norepinephrine as a possible synchronizer agent.

scholarly journals Daily Profile of glut1 and glut4 Expression in Tissues Inside and Outside the Blood-Brain Barrier in Control and Streptozotocin-Treated Rats

2013 ◽  
pp. S115-S124 ◽  
Author(s):  
D. ŠOLTÉSOVÁ ◽  
A. VESELÁ ◽  
B. MRAVEC ◽  
I. HERICHOVÁ
Keyword(s):  
Gene Expression ◽  
Blood Brain Barrier ◽  
Glucose Transporter ◽  
Diabetic Rats ◽  
Circadian System ◽  
Brain Barrier ◽  
Signal Molecule ◽  
Peripheral Oscillators ◽  
Glut4 Expression ◽  
Blood Brain

Glucose is molecule usually studied in relation to metabolism. Except for this traditional view, it is known that under certain conditions glucose can serve as a signal molecule for the circadian system. The circadian system is entrained by relevant synchronizing cues that can be tissue-dependent. Central oscillator is synchronized mainly by light-dark cycle, while peripheral oscillators can be entrained by food intake. Glucose transport in the organism is controlled by insulin dependent and independent mechanism. Therefore, we employed streptozotocin-induced diabetes to elucidate the influence of metabolic changes on glucose transporter (glut1, glut4) 24-h expression profile in peripheral oscillators in tissues, inside (frontal cortex, cerebellum) and outside (heart) the blood–brain barrier. Diabetes was induced by streptozotocin injection. Seventeen days later, sampling was performed during a 24-h cycle. Gene expression was measured using real-time PCR. We observed down-regulation of glut1 and glut4 expression in the heart of diabetic rats. The expression of glut1 and glut4 in brain areas was not down-regulated, however, we observed trend to phase advance in glut1 expression in the cerebellum. These results may indicate higher glucose levels in diabetic brain, which might influence regulation of clock gene expression in different manner in brain compared to periphery.

Protective effect of green tea extract against cadmium-induced testicular damage in rats in respect of oxidant/antioxidant equilibrium and androgen production

2020 ◽  
Vol 21 (1) ◽  
pp. 31-35
Author(s):  
Basma El-Desoky ◽  
Shaimaa El-Sayed ◽  
El-Said El-Said
Keyword(s):  
Gene Expression ◽  
Single Dose ◽  
Green Tea ◽  
Serum Testosterone ◽  
Green Tea Extract ◽  
Male Rats ◽  
Controlled Study ◽  
Control Group ◽  
Testicular Damage ◽  
Tea Extract

Objective: Investigating the effect of green tea extract (GTE) on the testicular damage induced by cadmium chloride CdCl2 in male rats. Design: Randomized controlled study. Animals: 40 male Wistar rats. Procedures: Rats were randomly divided into four groups: A) control group (each rat daily received pellet diet); B) GTE group each rat daily received pellet diet as well as 3 ml of 1.5 % w/v GTE, C) CdCl2 group each rat was I/P injected a single dose of 1 mg/kg CdCl2, then daily received pellet diet, and D) CdCl2+GTE group each rat was I/P injected a single dose of 1 mg/kg CdCl2 then daily received pellet diet as well as 3 ml of 1.5 % w/v GTE. After 30 days, blood samples were collected for hormonal assays (testosterone, FSH, and LH). In addition, both testes were collected; one of them was used for quantification of 17-beta hydroxysteroid dehydrogenase III (17β-HSDIII) gene expression using a real-time PCR. The other testis was used for determination of catalase and reduced glutathione; GSH, Nitric oxide (NO) and malondialdehyde (MDA) levels. Results: CdCl2 decreased serum testosterone levels and its synthesis pathway (17β-HSDIII testicular gene expression). While antioxidants catalase and GSH were reduced, oxidants MDA were enriched in the testes of CdCl2-poisoned rats. This CdCl2-promoted testicular dysfunction was corrected via the administration of GTE to male rats. Conclusion and clinical relevance: GTE could be used as a remedy for protecting against CdCl2-induced testicular damage in male rats.

The Protective Effect of Metformin against Oxandrolone-Induced Infertility in Male Rats

2020 ◽  
Vol 26 ◽  
Author(s):  
Abdulqader Fadhil Abed ◽  
Yazun Bashir Jarrar ◽  
Hamzeh J Al-Ameer ◽  
Wajdy Al-Awaida ◽  
Su-Jun Lee
Keyword(s):  
Gene Expression ◽  
Male Infertility ◽  
Protective Effect ◽  
Histological Examination ◽  
Sperm Count ◽  
Serum Testosterone ◽  
Male Rats ◽  
P Value ◽  
Protective Effects ◽  
Rt Pcr

Background: Oxandrolone is a synthetic testosterone analogue that is widely used among bodybuilders and athletes. However, oxandrolone causes male infertility. Recently, it was found that metformin reduces the risk of infertility associated with diabetes mellitus. Aim: This study aimed to investigate the protective effects of metformin against oxandrolone-induced infertility in male rats. Methods: Rats continuously received one of four treatments (n=7) over 14 days: control DMSO administration, oxandrolone administration, metformin administration, or co-administration of oxandrolone and metformin. Doses were equivalent to those used for human treatment. Subsequently, testicular and blood samples were collected for morphological, biochemical, and histological examination. In addition, gene expression of the testosterone synthesizing enzyme CYP11A1 was analyzed in the testes using RT-PCR. Results: Oxandrolone administration induced male infertility by significantly reducing relative weights of testes by 48%, sperm count by 82%, and serum testosterone levels by 96% (ANOVA, P value < 0.05). In addition, histological examination determined that oxandrolone caused spermatogenic arrest which was associated with 2-fold downregulation of testicular CYP11A1 gene expression. However, co-administration of metformin with oxandrolone significantly ameliorated toxicological alterations induced by oxandrolone exposure (ANOVA, P value < 0.05). Conclusion: Metformin administration protected against oxandrolone-induced infertility in male rats. Further clinical studies are needed to confirm the protective effect of metformin against oxandrolone-induced infertility among athletes.

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