Circadian Reprogramming by Timed Sodium Intake Reveals Transcriptional Pathways of Daily Salt Handling in the Colon.
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE280115 | GEO | 2025/10/31
REPOSITORIES: GEO
Similar Datasets
Project description:The circadian gene expression in peripheral tissue displays rhythmicity which is reprogrammed by feeding rhythms and dietary composition in mammals. In this study, circadian transcriptome was performed to investigate how the circadian clock and mineralocorticoid receptor contribute to daily gene expression in the colon.
2025-11-25 | GSE280123 | GEO
Project description:Circadian Reprogramming by Timed Sodium Intake Reveals Transcriptional Pathways of Daily Salt Handling in the Colon.
| PRJNA1176497 | ENA
Project description:Circadian Reprogramming by Timed Sodium Intake Reveals Transcriptional Pathways of Daily Salt Handling in the Colon.
| PRJNA1176500 | ENA
Project description:Daily rhythms in mammalian behaviour and physiology are generated by a multi-oscillator circadian system entrained through environmental cues (e.g. light and feeding). The presence of tissue niche-dependent physiological time cues has been proposed, allowing tissues the ability of circadian phase adjustment based on local signals. However, to date, such stimuli have remained elusive. Here we show that daily patterns of mechanical loading and associated osmotic challenge within physiological ranges reset circadian clock phase and amplitude in cartilage and intervertebral disc tissues in vivo and in tissue explant cultures. Hyperosmolarity (but not hypo-osmolarity) resets clocks in young and ageing skeletal tissues and induce genome-wide expression of rhythmic genes in cells. Mechanistically, RNAseq and biochemical analysis revealed the PLD2-mTORC2-AKT-GSK3β axis as a convergent pathway for both in vivo loading and hyperosmolarity-induced clock changes. These results reveal diurnal patterns of mechanical loading and consequent daily surges in osmolarity as a bona fide tissue niche-specific time cue to maintain skeletal circadian rhythms in sync.
2023-08-17 | E-MTAB-12877 | biostudies-arrayexpress
Project description:Circadian disruption has multiple pathological consequences, but the underlying mechanisms are largely unclear. To address such mechanisms, we subjected cultured cells to chronic circadian desynchrony (CCD), mimicking a chronic jet-lag paradigm, and assayed a range of cellular functions. The results indicated a specific circadian clock-dependent increase in cell proliferation. Transcriptome analysis revealed upregulation of G1-S-phase transition genes (cMyc, CyclinD1/3, Cdt1), concomitant with increased phosphorylation of the Retinoblastoma protein (Rb) by Cyclin D kinase 4/6 (CDK4/6) and increased G1-S progression. Phospho-Rb (Ser807/811) was found to oscillate in a circadian fashion and exhibit phase-shifted rhythms in circadian desynchronized cells. A CDK4/6 inhibitor approved for cancer treatment reduced growth of cultured cells and mouse tumors in a time-of-day specific manner, but the time dependence was lost with CCD. Our study identifies a mechanism that underlies effects of circadian disruption on tumor growth and underscores the importance of treatment timed to endogenous circadian rhythms.
2019-05-14 | GSE119668 | GEO
Project description:The circadian system plays an essential role in regulating timing of body metabolism in humans. Indeed, circadian misalignments are strongly associated with high rates of metabolic disorders. Molecular makeup of the circadian oscillator can be deciphered in cells cultured in vitro, and these cellular rhythms are highly informative of the physiological circadian rhythm in vivo.
We aimed at assessing molecular clock properties in dermal fibroblasts established from the skin biopsies of seventeen Type 2 diabetic obese and non-obese patients and eleven healthy controls. Following in vitro synchronization, primary fibroblast cultures were subjected to continuous assessment of circadian bioluminescence profiles based on lentiviral luciferase reporters.
We observed a strong inverse correlation between HbA1c values and circadian period length within cells from the Type 2 diabetic group. RNA sequencing analysis conducted in this group samples revealed that ICAM1 encoding for the endothelial adhesion protein was differentially expressed between Type 2 diabetic compensated and non-compensated fibroblasts, and correlated with the period length. Furthermore, ICAM1 expression is driven by rhythmic CLOCK binding.
We provide for the first time a potential molecular link between severity of Type 2 diabetes and circadian clock machinery, which paves a way for further mechanistic understanding of circadian oscillator changes upon Type 2 diabetes in humans.
| EGAS00001003622 | EGA
Project description:High salt intake is a major risk factor for hypertension. Although acute caffeine intake produces moderate diuresis and natriuresis, caffeine increases the blood pressure (BP) through activating sympathetic activity. However, the long-term effects of caffeine on urinary sodium excretion and blood pressure are rarely investigated. Here, we investigated whether chronic caffeine administration antagonizes salt sensitive hypertension by promoting urinary sodium excretion. Dahl salt-sensitive (Dahl-S) rats were fed with high salt diet with or without 0.1% caffeine in drinking water for 15 days. The BP, heart rate and locomotor activity of rats was analyzed and urinary sodium excretion was determined. The renal epithelial Na(+) channel (ENaC) expression and function were measured by in vivo and in vitro experiments. Chronic consumption of caffeine attenuates hypertension induced by high salt without affecting sympathetic nerve activity in Dahl-S rats. The renal α-ENaC expression and ENaC activity of rats decreased after chronic caffeine administration. Caffeine increased phosphorylation of AMPK and decrease α-ENaC expression in cortical collecting duct cells. Inhibiting AMPK abolished the effect of caffeine on α-ENaC. Chronic caffeine intake prevented the development of salt-sensitive hypertension through promoting urinary sodium excretion, which was associated with activation of renal AMPK and inhibition of renal tubular ENaC.
| S-EPMC4866033 | biostudies-literature
Project description:The circadian clock is comprised of proteins that form negative feedback loops, which regulate the timing of global gene expression in a coordinated 24 hour cycle. As a result, the plant circadian clock is responsible for regulating numerous physiological processes central to growth and survival. To date, most plant circadian clock studies have relied on diurnal transcriptome changes to elucidate molecular connections between the circadian clock and observable phenotypes in wild-type plants. Here, we have combined high-throughput RNA-sequencing and mass spectrometry to comparatively characterize the lhycca1, prr7prr9, gi and toc1 circadian clock mutant rosette transcriptome and proteome at the end-of-day and end-of-night.
2018-01-02 | PXD004763 | Pride
Project description:Regular exercise is important for physical and mental health. An underexplored and intriguing property of exercise is its actions on the body's 24 h or circadian rhythms. Molecular clock cells in the brain's suprachiasmatic nuclei (SCN) use electrical and chemical signals to orchestrate their activity and convey time of day information to the rest of the brain and body. To date, the long-lasting effects of regular physical exercise on SCN clock cell coordination and communication remain unresolved. Utilizing mouse models in which SCN intercellular neuropeptide signaling is impaired as well as those with intact SCN neurochemical signaling, we examined how daily scheduled voluntary exercise (SVE) influenced behavioral rhythms and SCN molecular and neuronal activities. We show that in mice with disrupted neuropeptide signaling, SVE promotes SCN clock cell synchrony and robust 24 h rhythms in behavior. Interestingly, in both intact and neuropeptide signaling deficient animals, SVE reduces SCN neural activity and alters GABAergic signaling. These findings illustrate the potential utility of regular exercise as a long-lasting and effective non-invasive intervention in the elderly or mentally ill where circadian rhythms can be blunted and poorly aligned to the external world.
| S-EPMC8213798 | biostudies-literature
Project description:The body's circadian rhythm is coordinated by a central hypothalamic and peripheral molecular clocks, which involve clock proteins (PER, CRY, CLOCK, and BMAL1). Our recent study demonstrated that deletion of Per1 in Dahl salt-sensitive (SS) rats (SSPer1-/-) exacerbated SS hypertension (HTN), kidney injury, and disrupted blood pressure rhythms. To define time-of-day, genotype-, and diet-dependent alterations in the renal transcriptome and proteome associated with SS HTN, we collected kidney cortex from SS and SSPer1-/- rats fed either a normal salt (NS, 0.4% NaCl) or high salt (HS, 4% NaCl) diet. Samples were obtained during both the active (night) and inactive (day) phases. The diet challenges were conducted for 3 weeks in male rats. Bulk RNA-sequencing was performed on both NS and HS-fed groups, and proteomic analyses were performed in HS-fed groups. In SS rats, HS intake markedly blunted time-of-day-dependent transcriptional changes, including reduced differential expression of core circadian genes such as Bmal1 and Nr1d1 when transitioning from the inactive to the active phase. Pathway analyses revealed significant stress and immune response, as well as metabolic adaptations caused by the HS diet. Specifically, the remodeling of the pyruvate dehydrogenase complex was identified as a key prediction in both transcriptomic and phosphoproteomic datasets. As anticipated, Per1 deletion further exacerbated disruptions in immune regulation and metabolic adaptation. Collectively, our findings demonstrate that numerous renal genes exhibit diurnal oscillations under physiological conditions and are profoundly disrupted in SS HTN, likely contributing to impaired kidney function and circadian misalignment of blood pressure regulation.
2025-12-01 | GSE311806 | GEO