Astrocytes in the mouse suprachiasmatic nuclei respond directly to glucocorticoids feedback
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ABSTRACT:
PROVIDER: PRJNA1005276 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR25634653_1.fastq.gz | Fastqsanger.gz | |||
| SRR25634653_2.fastq.gz | Fastqsanger.gz | |||
| SRR25634654_1.fastq.gz | Fastqsanger.gz | |||
| SRR25634654_2.fastq.gz | Fastqsanger.gz | |||
| SRR25634655_1.fastq.gz | Fastqsanger.gz |
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Project description:The circadian timing system anticipates daily recurring changes in the environment to synchronize physiology. In mammals, the master pacemaker is the hypothalamic suprachiasmatic nuclei (SCN), which synchronizes “wake” functions by inducing the circadian release of Glucocorticoids (GCs) from the adrenal gland. GCs peak right before the active phase and set the time of peripheral clocks, however, it is still unclear whether the SCN respond to GCs feedback. While GCs influence directly the SCN during the perinatal period, the adult circuit is considered to be resistant to them, suggesting a reduction of GCs-sensitivity along development. To understand this mechanism, we followed the expression of GC receptor (GR) along mouse SCN development with single cell resolution and show that GR is up-regulated in astrocytes as the circuit matures. We provide in vivo and in vitro evidence that the adult SCN stays responsive to circulating GCs through the activation of GR in astrocytes. Astrocytes’ communication is necessary to induce the GC-dependent shift on the SCN clock. Our data provides insight into the development of the SCN and highlight a new role of astrocytes as time-keepers in the adult. This finding might shed light on how the circadian system adapts to jetlag or shift work.
2024-04-10 | GSE240803 | GEO
Project description:Mice lacking the stem/progenitor cell transcription factor, Sex determining region Y-box 2 (SOX2), in neurons of the suprachiasmatic nuclei display imprecise, poorly consolidated behavioral rhythms that do not entrain efficiently to environmental light cycles. RNA sequencing revealed that Sox2 deficiency alters the circadian transcriptome of the SCN, reducing the expression of many core clock genes and neuropeptide-receptor systems.
2019-03-18 | E-MTAB-7496 | biostudies-arrayexpress
Project description:We report circadian (time series, circadian time 0, 3, 6, 9, 12, 18, 21h) transcriptomic analysis of mouse fetal (embryonic day 17) suprachiasmatic nuclei (SCN) from either sham operarated ad libitum fed mothers (group A) or from SCN-lesioned mothers on resctricted feeding regime. The analysis revealed low amplitude rhythms in the fetal SCN driven by maternal SCN and/or maternal feeding behavior.
2022-04-01 | GSE183172 | GEO
Project description:Glucocorticoids are the cornerstone of asthma and other inflammatory disease therapy. Resistance or insensitivity to glucocorticoids presents a substantial and challenging clinical problem. MicroRNAs are emerging as central regulators of inflammation, but it is not clear whether they could augment or attenuate glucocorticoid responses. We aimed to identify microRNAs that regulate cytokine and chemokine expression in airway epithelial cells and whether these miRNAs are subject to the effects of glucocorticoids. MicroRNAomic analyses of primary bronchial epithelial cells and the A549 airway epithelial cell line identified 7 miRNAs that were altered by inflammatory cytokine treatment and 22 that were regulated by glucocorticoids (n=3 for each treatment). miR-146a emerged as a central candidate, whose expression was induced by TNF-alpha and repressed by glucocorticoids. Its role as a candidate in asthmatic inflammation was supported by expression profiling in human asthmatics, which showed that plasma miR-146a expression was elevated in asthma and associated with measures related to worse asthma outcomes, including elevated blood eosinophil counts, higher asthma control questionnaire scores, and need for higher doses of inhaled glucocorticoids. However, transfection of miR-146a in A549 cells treated with TNF-alpha +/- glucocorticoids produced an anti-inflammatory effect and with increased efficacy of glucocorticoids. We propose a model whereby miR-146a is induced by inflammatory conditions as a feedback mechanism to limit inflammation. Glucocorticoids may limit this regulatory pathway by preventing miR-146a expression. Consequently, exogenous administration of miR-146a could be a novel therapeutic strategy to enhance effects of glucocorticoids.
2018-11-01 | GSE120758 | GEO
Project description:Although the mammalian rest-activity cycle is controlled by a "master clock" in the suprachiasmatic nuclei (SCN) of the hypothalamus, it is unclear how firing of individual SCN neurons gates individual features of daily activity. Here, we demonstrate that a specific transcriptomically identified population of mouse VIP+ SCN neurons is active at the "wrong" time of the day -nighttime- when most SCN neurons are silent. Using chemogenetic and optogenetic strategies, we show that these neurons and their cellular clocks are necessary and sufficient to gate and time nighttime sleep, but have no effect upon daytime sleep. We propose mouse nighttime sleep, analogous to the human siesta, is a "hard-wired" property gated by specific neurons of the master clock to favor subsequent alertness prior to dawn (a circadian "wake maintenance zone"). Thus, the SCN is not simply a 24h metronome: specific populations sculpt critical features of the sleep-wake cycle.
2021-01-21 | GSE154038 | GEO
Project description:Males and females exhibit differences in the incidence of many major diseases including auto-immune diseases, hepatocellular carcinoma, diabetes, and osteoporosis, which all have important inflammatory components in their etiology. Glucocorticoids are the primary physiological anti-inflammatory hormone in all mammals and synthetic derivatives of these hormones are widely prescribed as anti-inflammatory agents irrespective of gender. Surprisingly we report a marked sexually dimorphic regulation of gene expression by glucocorticoids in the rat liver. Eight distinct patterns of glucocorticoid regulated genes were identified and two revealed genes that respond to glucocorticoid treatment in both sexes in opposite directions (anti-correlated genes. We also identified gender-specific groups of genes regulated by glucocorticoids. Pathways analysis identified sex-specific glucocorticoid regulated gene expression in several canonical pathways that have been implicated in human disease in which disease susceptibility is sex-biased. For example, comparison of number of genes involved in inflammatory disorders between sexes, revealed 84 additional glucocorticoid responsive genes in the male rat. Our data suggests that glucocorticoids thorough sexually-dimorphic regulation of gene expression modulate gender specific homeostatic functions in male and female liver.
2010-10-02 | GSE13461 | GEO
Project description:Circadian VIPergic neurons of the suprachiasmatic nuclei sculpt the sleep-wake cycle
| PRJNA644912 | ENA
Project description:Males and females exhibit differences in the incidence of many major diseases including auto-immune diseases, hepatocellular carcinoma, diabetes, and osteoporosis, which all have important inflammatory components in their etiology. Glucocorticoids are the primary physiological anti-inflammatory hormone in all mammals and synthetic derivatives of these hormones are widely prescribed as anti-inflammatory agents irrespective of gender. Surprisingly we report a marked sexually dimorphic regulation of gene expression by glucocorticoids in the rat liver. Eight distinct patterns of glucocorticoid regulated genes were identified and two revealed genes that respond to glucocorticoid treatment in both sexes in opposite directions (anti-correlated genes. We also identified gender-specific groups of genes regulated by glucocorticoids. Pathways analysis identified sex-specific glucocorticoid regulated gene expression in several canonical pathways that have been implicated in human disease in which disease susceptibility is sex-biased. For example, comparison of number of genes involved in inflammatory disorders between sexes, revealed 84 additional glucocorticoid responsive genes in the male rat. Our data suggests that glucocorticoids thorough sexually-dimorphic regulation of gene expression modulate gender specific homeostatic functions in male and female liver. Adult males and females adrenalectomized Sprague-Dawley rats (8-10 weeks of age) (females Distrous 1) were treated with vehicle (Phosphate Buffered Saline – 400 µl) or Dexamethasone (1mg/Kg i.p.) purchased from Steraloids (Newport, RI). Liver was harvested 6 hours after treatment and kept in RNA later solution at 4oC over night. Samples were frozen and stored at -80oC. Three replicate microarrays were completed for each group (male vehicle, male dexamethasone, female vehicle and female dexamethasone) for a total of 12 microarrays. Each microarray was hybridized using a pooled RNA sample, and each pool was created from equal amounts of total RNA from three independent RNA samples, representing individual animals (n=9 animals per group). This approach provides appropriate biological replication within the constraints of a limiting number of microarrays (C. Kendziorski, R. A. Irizarry, K. S. Chen, J. D. Haag, M. N. Gould, Proc Natl Acad Sci U S A 102, 4252 Mar 22, 2005).
2010-10-01 | E-GEOD-13461 | biostudies-arrayexpress
Project description:In mice and other mammals the suprachiasmatic nuclei (SCN) within the brain, synchronises daily rhythms in metabolism, physiology and behaviour to the Earth's local time. Whilst much is known about the SCN's time keeping mechanism, less is known about how it adjusts or resets timing to changes in local time beyond the induction of CRE regulated genes and the differential response of dorsal and ventral sub-regions of the SCN after light exposure known to advance rhythms. As transcription of several clock genes is required for maintaining daily rhythms, we assayed global transcription levels in the dorsal, ventral and central SCN following phase advance inducing light exposure to expand understanding of how the SCN adjusts to new local times.
2019-01-01 | GSE53553 | GEO
Project description:A direct retinal projection targets the suprachiasmatic nucleus (SCN) (an important hypothalamic control center). The accepted function of this projection is to convey information about ambient light (irradiance) to synchronize the SCN's endogenous circadian clock with local time and drive the diurnal variations in physiology and behavior [1-4]. Here, we report that it also renders the SCN responsive to visual images. We map spatial receptive fields (RFs) for SCN neurons and find that only a minority are excited (or inhibited) by light from across the scene as expected for irradiance detectors. The most commonly encountered units have RFs with small excitatory centers, combined with very extensive inhibitory surrounds that reduce their sensitivity to global changes in light in favor of responses to spatial patterns. Other units have larger excitatory RF centers, but these always cover a coherent region of visual space, implying visuotopic order at the single-unit level. Approximately 75% of light-responsive SCN units modulate their firing according to simple spatial patterns (drifting or inverting gratings) without changes in irradiance. The time-averaged firing rate of the SCN is modestly increased under these conditions, but including spatial contrast did not significantly alter the circadian phase resetting efficiency of light. Our data indicate that the SCN contains information about irradiance and spatial patterns. This newly appreciated sensory capacity provides a mechanism by which behavioral and physiological systems downstream of the SCN could respond to visual images [5].
| S-EPMC5462621 | biostudies-literature