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Author van der Burght, B.W.; Hansen, M.; Olsen, J.; Zhou, J.; Wu, Y.; Nissen, M.H.; Sparrow, J.R.
Title Early changes in gene expression induced by blue light irradiation of A2E-laden retinal pigment epithelial cells Type Journal Article
Year 2013 Publication (up) Acta Ophthalmologica Abbreviated Journal Acta Ophthalmol
Volume 91 Issue 7 Pages e537-45
Keywords Apoptosis; Cell Line; Cell Survival; Gene Expression Regulation/*physiology; Humans; Light; Lipofuscin/genetics; Oligonucleotide Array Sequence Analysis; Principal Component Analysis; Pyridinium Compounds; RNA, Messenger/genetics; Real-Time Polymerase Chain Reaction; Retinal Pigment Epithelium/metabolism/pathology/*radiation effects; Retinoids/*genetics; Transcriptome; A2e; age-related macular degeneration; apoptosis; complement cascade; gene expression; retinal pigment epithelial cells; blue light; retinal pigment epithelial; epigenetics
Abstract PURPOSE: Accumulation of bisretinoids as lipofuscin in retinal pigment epithelial (RPE) cells is implicated in the pathogenesis of some blinding diseases including age-related macular degeneration (AMD). To identify genes whose expression may change under conditions of bisretinoid accumulation, we investigated the differential gene expression in RPE cells that had accumulated the lipofuscin fluorophore A2E and were exposed to blue light (430 nm). METHODS: A2E-laden RPE cells were exposed to blue light (A2E/430 nm) at various time intervals. Cell death was quantified using Dead Red staining, and RNA levels for the entire genome was determined using DNA microarrays (Affymetrix GeneChip Human Genome 2.0 Plus). Array results for selected genes were confirmed by real-time reverse-transcriptase polymerase chain reaction. RESULTS: Principal component analysis revealed that the A2E-laden RPE cells irradiated with blue light were clearly distinguishable from the control samples. We found differential regulation of genes belonging to the following functional groups: transcription factors, stress response, apoptosis and immune response. Among the last mentioned were downregulation of four genes that coded for proteins that have an inhibitory effect on the complement cascade: (complement factor H, complement factor H-related 1, complement factor I and vitronectin) and of two belonging to the classical pathway (complement component 1, s subcomponent and complement component 1, r subcomponent). CONCLUSION: This study demonstrates that blue light irradiation of A2E-laden RPE cells can alter the transcription of genes belonging to different functional pathways including stress response, apoptosis and the immune response. We suggest that these molecules may be associated to the pathogenesis of AMD and can potentially serve as future therapeutic targets.
Address Department of International Health, Immunology and Microbiology, Eye Research Unit, University of Copenhagen, Copenhagen, DenmarkDepartment of Cellular and Molecular Medicine, University of Copenhagen, Copenhagen, DenmarkDepartment of Ophthalmology, Columbia University, New York, New York, USA
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1755-375X ISBN Medium
Area Expedition Conference
Notes PMID:23742627 Approved no
Call Number IDA @ john @ Serial 346
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Author Brady, A.; Willis, B.; Harder, L.; Vizel, P.
Title Lunar Phase Modulates Circadian Gene Expression Cycles in the Broadcast Spawning Coral Acropora millepora Type Journal Article
Year 2016 Publication (up) Biological Bulletin Abbreviated Journal Biol Bullet
Volume 230 Issue 2 Pages 130-142
Keywords Animals; corals; Acropora millepora; lunar cycle; Circadian Rhythm; gene expression; moon
Abstract Many broadcast spawning corals in multiple reef regions release their gametes with incredible temporal precision just once per year, using the lunar cycle to set the night of spawning. Moonlight, rather than tides or other lunar-regulated processes, is thought to be the proximate factor responsible for linking the night of spawning to the phase of the Moon. We compared patterns of gene expression among colonies of the broadcast spawning coral Acropora millepora at different phases of the lunar cycle, and when they were maintained under one of three experimentally simulated lunar lighting treatments: i) lunar lighting conditions matching those on the reef, or lunar patterns mimicking either ii) constant full Moon conditions, or iii) constant new Moon conditions. Normal lunar illumination was found to shift both the level and timing of clock gene transcription cycles between new and full moons, with the peak hour of expression for a number of genes occurring earlier in the evening under a new Moon when compared to a full Moon. When the normal lunar cycle is replaced with nighttime patterns equivalent to either a full Moon or a new Moon every evening, the normal monthlong changes in the level of expression are destroyed for most genes. In combination, these results indicate that daily changes in moonlight that occur over the lunar cycle are essential for maintaining normal lunar periodicity of clock gene transcription, and this may play a role in regulating spawn timing. These data also show that low levels of light pollution may have an impact on coral biological clocks.
Address Department of Biological Science, University of Calgary, 2500 University Drive NW, Calgary, Alberta T2N 1N4, Canada; pvize(at)ucalgary.ca
Corporate Author Thesis
Publisher Marine Biological Laboratory Place of Publication Editor
Language English Summary Language English Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 1476
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Author Kavcic, P.; Rojc, B.; Dolenc-Groselj, L.; Claustrat, B.; Fujs, K.; Poljak, M.
Title The impact of sleep deprivation and nighttime light exposure on clock gene expression in humans Type Journal Article
Year 2011 Publication (up) Croatian Medical Journal Abbreviated Journal Croat Med J
Volume 52 Issue 5 Pages 594-603
Keywords genomics; epigenetics; hPer2; hBmal1; clock genes; gene expression; biology; human health
Abstract Aim

To examine the effect of acute sleep deprivation under light conditions on the expression of two key clock genes, hPer2 and hBmal1, in peripheral blood mononuclear cells (PBMC) and on plasma melatonin and cortisol levels.

Methods

Blood samples were drawn from 6 healthy individuals at 4-hour intervals for three consecutive nights, including a night of total sleep deprivation (second night). The study was conducted in April-June 2006 at the University Medical Centre Ljubljana.

Results

We found a significant diurnal variation in hPer2 and hBmal1 expression levels under baseline (P < 0.001, F = 19.7, df = 30 for hPer2 and P < 0.001, F = 17.6, df = 30 for hBmal1) and sleep-deprived conditions (P < 0.001, F = 9.2, df = 30 for hPer2 and P < 0.001, F = 13.2, df = 30 for hBmal1). Statistical analysis with the single cosinor method revealed circadian variation of hPer2 under baseline and of hBmal1 under baseline and sleep-deprived conditions. The peak expression of hPer2 was at 13:55 ± 1:15 hours under baseline conditions and of hBmal1 at 16:08 ± 1:18 hours under baseline and at 17:13 ± 1:35 hours under sleep-deprived conditions. Individual cosinor analysis of hPer2 revealed a loss of circadian rhythm in 3 participants and a phase shift in 2 participants under sleep-deprived conditions. The plasma melatonin and cortisol rhythms confirmed a conventional alignment of the central circadian pacemaker to the habitual sleep/wake schedule.

Conclusion

Our results suggest that 40-hour acute sleep deprivation under light conditions may affect the expression of hPer2 in PBMCs.
Address
Corporate Author Thesis
Publisher Place of Publication Editor
Language Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0353-9504 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number IDA @ john @ Serial 135
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Author Fonken, L.K.; Lieberman, R.A.; Weil, Z.M.; Nelson, R.J.
Title Dim light at night exaggerates weight gain and inflammation associated with a high-fat diet in male mice Type Journal Article
Year 2013 Publication (up) Endocrinology Abbreviated Journal Endocrinology
Volume 154 Issue 10 Pages 3817-3825
Keywords Adipose Tissue, White/*immunology/metabolism/pathology; Animals; Antigens, CD11b/biosynthesis/genetics/metabolism; Appetite Regulation/*radiation effects; Arcuate Nucleus/*immunology/metabolism/pathology; Behavior, Animal/radiation effects; Circadian Rhythm; Cytokines/biosynthesis/genetics/metabolism; Diet, High-Fat/*adverse effects; Feeding Behavior/radiation effects; Gene Expression Regulation; Glucose Intolerance/etiology/immunology/metabolism/pathology; I-kappa B Kinase/biosynthesis/genetics/metabolism; Insulin Resistance; Lighting/*adverse effects; Male; Mice; Microglia/immunology/metabolism/pathology; Nerve Tissue Proteins/biosynthesis/genetics/metabolism; Obesity/*etiology/immunology/metabolism/pathology; Random Allocation; *Weight Gain
Abstract Elevated nighttime light exposure is associated with symptoms of metabolic syndrome. In industrialized societies, high-fat diet (HFD) and exposure to light at night (LAN) often cooccur and may contribute to the increasing obesity epidemic. Thus, we hypothesized that dim LAN (dLAN) would provoke additional and sustained body mass gain in mice on a HFD. Male mice were housed in either a standard light/dark cycle or dLAN and fed either chow or HFD. Exposure to dLAN and HFD increase weight gain, reduce glucose tolerance, and alter insulin secretion as compared with light/dark cycle and chow, respectively. The effects of dLAN and HFD appear additive, because mice exposed to dLAN that were fed HFD display the greatest increases in body mass. Exposure to both dLAN and HFD also change the timing of food intake and increase TNFalpha and MAC1 gene expression in white adipose tissue after 4 experimental weeks. Changes in MAC1 gene expression occur more rapidly due to HFD as compared with dLAN; after 5 days of experimental conditions, mice fed HFD already increase MAC1 gene expression in white adipose tissue. HFD also elevates microglia activation in the arcuate nucleus of the hypothalamus and hypothalamic TNFalpha, IL-6, and Ikbkb gene expression. Microglia activation is increased by dLAN, but only among chow-fed mice and dLAN does not affect inflammatory gene expression. These results suggest that dLAN exaggerates weight gain and peripheral inflammation associated with HFD.
Address Department of Neuroscience, Wexner Medical Center, The Ohio State University, 636 Biomedical Research Tower, 460 West 12th Avenue, Columbus, Ohio 43210. fonken.1@osu.edu
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 0013-7227 ISBN Medium
Area Expedition Conference
Notes PMID:23861373 Approved no
Call Number IDA @ john @ Serial 93
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Author Kovac, J.; Husse, J.; Oster, H.
Title A time to fast, a time to feast: the crosstalk between metabolism and the circadian clock Type Journal Article
Year 2009 Publication (up) Molecules and Cells Abbreviated Journal Mol Cells
Volume 28 Issue 2 Pages 75-80
Keywords Human Health; Animals; Biological Clocks/*physiology; CLOCK Proteins/genetics/metabolism; Circadian Rhythm/*physiology; Energy Metabolism/*physiology; Gene Expression Regulation; Homeostasis; Humans; Period Circadian Proteins/genetics/metabolism; Time Factors
Abstract The cyclic environmental conditions brought about by the 24 h rotation of the earth have allowed the evolution of endogenous circadian clocks that control the temporal alignment of behaviour and physiology, including the uptake and processing of nutrients. Both metabolic and circadian regulatory systems are built upon a complex feedback network connecting centres of the central nervous system and different peripheral tissues. Emerging evidence suggests that circadian clock function is closely linked to metabolic homeostasis and that rhythm disruption can contribute to the development of metabolic disease. At the same time, metabolic processes feed back into the circadian clock, affecting clock gene expression and timing of behaviour. In this review, we summarize the experimental evidence for this bimodal interaction, with a focus on the molecular mechanisms mediating this exchange, and outline the implications for clock-based and metabolic diseases.
Address Circadian Rhythms Group, Max Planck Institute of Biophysical Chemistry, 37077, Gottingen, Germany
Corporate Author Thesis
Publisher Place of Publication Editor
Language English Summary Language Original Title
Series Editor Series Title Abbreviated Series Title
Series Volume Series Issue Edition
ISSN 1016-8478 ISBN Medium
Area Expedition Conference
Notes PMID:19714310 Approved no
Call Number LoNNe @ kagoburian @ Serial 772
Permanent link to this record