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Author Dunlap, J.C.
Title Molecular Bases for Circadian Clocks Type Journal Article
Year 1999 Publication (up) Cell Abbreviated Journal Cell
Volume 96 Issue 2 Pages 271-290
Keywords Human Health; Animals; Ecology
Abstract
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 0092-8674 ISBN Medium
Area Expedition Conference
Notes Approved no
Call Number LoNNe @ kagoburian @ Serial 737
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Author Welz, P.-S.; Zinna, V.M.; Symeonidi, A.; Koronowski, K.B.; Kinouchi, K.; Smith, J.G.; Guillen, I.M.; Castellanos, A.; Crainiciuc, G.; Prats, N.; Caballero, J.M.; Hidalgo, A.; Sassone-Corsi, P.; Benitah, S.A.
Title BMAL1-Driven Tissue Clocks Respond Independently to Light to Maintain Homeostasis Type Journal Article
Year 2019 Publication (up) Cell Abbreviated Journal Cell
Volume 177 Issue 6 Pages 1436-1447.e12
Keywords Animals
Abstract Circadian rhythms control organismal physiology throughout the day. At the cellular level, clock regulation is established by a self-sustained Bmal1-dependent transcriptional oscillator network. However, it is still unclear how different tissues achieve a synchronized rhythmic physiology. That is, do they respond independently to environmental signals, or require interactions with each other to do so? We show that unexpectedly, light synchronizes the Bmal1-dependent circadian machinery in single tissues in the absence of Bmal1 in all other tissues. Strikingly, light-driven tissue autonomous clocks occur without rhythmic feeding behavior and are lost in constant darkness. Importantly, tissue-autonomous Bmal1 partially sustains homeostasis in otherwise arrhythmic and prematurely aging animals. Our results therefore support a two-branched model for the daily synchronization of tissues: an autonomous response branch, whereby light entrains circadian clocks without any commitment of other Bmal1-dependent clocks, and a memory branch using other Bmal1-dependent clocks to “remember” time in the absence of external cues.
Address Institute for Research in Biomedicine (IRB Barcelona), Barcelona Institute of Science and Technology, 08028 Barcelona, Spain; ICREA, Catalan Institution for Research and Advanced Studies, 08010 Barcelona, Spain. Electronic address: salvador.aznar-benitah@irbbarcelona.org
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 0092-8674 ISBN Medium
Area Expedition Conference
Notes PMID:31150620 Approved no
Call Number GFZ @ kyba @ Serial 2513
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Author Bapary, M.A.J.; Takano, J.-I.; Soma, S.; Sankai, T.
Title Effect of blue LED light and antioxidants potential in a somatic cell Type Journal Article
Year 2019 Publication (up) Cell Biology International Abbreviated Journal Cell Biol Int
Volume 43 Issue 11 Pages 1296-1306
Keywords Cells; Biology; LED; blue light; Antioxidants; cell death
Abstract Light is an indispensable part of routine laboratory works in which conventional light is generally used. Light-emitting diodes (LEDs) have come to replace the conventional light thus could be a potent target in biomedical studies. Since blue light is a major component of visible light wavelength, in this study, using a somatic cell from African green monkey kidney, we assessed the possible consequences of blue spectra of LED light in future animal experiments and proposed a potent mitigation against light induced damages. COS-7 cells were exposed to blue LED light (450 nm) and the growth and DNA damage were assessed at different exposure times. A higher suppression in cell growth and viability was observed under a longer period of blue LED light exposure. The number of apoptotic cells increased as light exposure time was prolonged. Reactive oxygen species generation was also elevated in accordance to the extension of light exposure times. A comparison to dark-maintained cells revealed that the upregulation of ROS by blue LED light plays a significant role in causing cellular dysfunction in DNA in a time-dependent manner. In turn, antioxidant treatment has shown to improve the cell growth and viability under blue LED light conditions. This indicates that antioxidants are potential against blue LED light-induced somatic cell damage. It is expected that this study will contribute to the understanding of the basic mechanism of somatic cell death under visible light and to maximize the beneficial use of LED light in future animal experiments.
Address Tsukuba Primate Research Center, National Institutes of Biomedical Innovation, Health and Nutrition, Ibaraki, Japan
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 1065-6995 ISBN Medium
Area Expedition Conference
Notes PMID:30958611 Approved no
Call Number GFZ @ kyba @ Serial 2328
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Author Pan, Y.-R.; Song, J.-Y.; Fan, B.; Wang, Y.; Che, L.; Zhang, S.-M.; Chang, Y.-X.; He, C.; Li, G.-Y.
Title mTOR may interact with PARP-1 to regulate visible light-induced parthanatos in photoreceptors Type Journal Article
Year 2020 Publication (up) Cell Communication and Signaling : CCS Abbreviated Journal Cell Commun Signal
Volume 18 Issue 1 Pages 27
Keywords Health; Aif; Parp-1; Parthanatos; Retinal neuroprotection; Sirt1; mTOR
Abstract BACKGROUND: Excessive light exposure is a detrimental environmental factor that plays a critical role in the pathogenesis of retinal degeneration. However, the mechanism of light-induced death of retina/photoreceptor cells remains unclear. The mammalian/mechanistic target of rapamycin (mTOR) and Poly (ADP-ribose) polymerase-1 (PARP-1) have become the primary targets for treating many neurodegenerative disorders. The aim of this study was to elucidate the mechanisms underlying light-induced photoreceptor cell death and whether the neuroprotective effects of mTOR and PARP-1 inhibition against death are mediated through apoptosis-inducing factor (AIF). METHODS: Propidium iodide (PI)/Hoechst staining, lentiviral-mediated short hairpin RNA (shRNA), Western blot analysis, cellular fraction separation, plasmid transient transfection, laser confocal microscopy, a mice model, electroretinography (ERG), and hematoxylin-eosin (H & E) staining were employed to explore the mechanisms by which rapamycin/3-Aminobenzamide (3AB) exert neuroprotective effects of mTOR/PARP-1 inhibition in light-injured retinas. RESULTS: A parthanatos-like death mechanism was evaluated in light-injured 661 W cells that are an immortalized photoreceptor-like cell line that exhibit cellular and biochemical feature characteristics of cone photoreceptor cells. The death process featured over-activation of PARP-1 and AIF nuclear translocation. Either PARP-1 or AIF knockdown played a significantly protective role for light-damaged photoreceptors. More importantly, crosstalk was observed between mTOR and PARP-1 signaling and mTOR could have regulated parthanatos via the intermediate factor sirtuin 1 (SIRT1). The parthanatos-like injury was also verified in vivo, wherein either PARP-1 or mTOR inhibition provided significant neuroprotection against light-induced injury, which is evinced by both structural and functional retinal analysis. Overall, these results elucidate the mTOR-regulated parthanatos death mechanism in light-injured photoreceptors/retinas and may facilitate the development of novel neuroprotective therapies for retinal degeneration diseases. CONCLUSIONS: Our results demonstrate that inhibition of the mTOR/PARP-1 axis exerts protective effects on photoreceptors against visible-light-induced parthanatos. These protective effects are conducted by regulating the downstream factors of AIF, while mTOR possibly interacts with PARP-1 via SIRT1 to regulate parthanatos. Video Abstract Schematic diagram of mTOR interacting with PARP-1 to regulate visible light-induced parthanatos. Increased ROS caused by light exposure penetrates the nuclear membrane and causes nuclear DNA strand breaks. PARP-1 detects DNA breaks and synthesizes PAR polymers to initiate the DNA repair system that consumes a large amount of cellular NAD+. Over-production of PAR polymers prompts the release of AIF from the mitochondria and translocation to the nucleus, which leads to parthanatos. Activated mTOR may interact with PARP-1 via SIRT1 to regulate visible light-induced parthanatos.
Address Department of Ophthalmology, Second Hospital of JiLin University, No.218 Zi-Qiang St, ChangChun, 130041, China. liguangyu@aliyun.com
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 1478-811X ISBN Medium
Area Expedition Conference
Notes PMID:32066462 Approved no
Call Number GFZ @ kyba @ Serial 2830
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Author Papagiannakopoulos, T.; Bauer, M.R.; Davidson, S.M.; Heimann, M.; Subbaraj, L.; Bhutkar, A.; Bartlebaugh, J.; Vander Heiden, M.G.; Jacks, T.
Title Circadian Rhythm Disruption Promotes Lung Tumorigenesis Type Journal Article
Year 2016 Publication (up) Cell Metabolism Abbreviated Journal Cell Metab
Volume 24 Issue 2 Pages 324–331
Keywords Animals
Abstract Circadian rhythms are 24-hr oscillations that control a variety of biological processes in living systems, including two hallmarks of cancer, cell division and metabolism. Circadian rhythm disruption by shift work is associated with greater risk for cancer development and poor prognosis, suggesting a putative tumor-suppressive role for circadian rhythm homeostasis. Using a genetically engineered mouse model of lung adenocarcinoma, we have characterized the effects of circadian rhythm disruption on lung tumorigenesis. We demonstrate that both physiologic perturbation (jet lag) and genetic mutation of the central circadian clock components decreased survival and promoted lung tumor growth and progression. The core circadian genes Per2 and Bmal1 were shown to have cell-autonomous tumor-suppressive roles in transformation and lung tumor progression. Loss of the central clock components led to increased c-Myc expression, enhanced proliferation, and metabolic dysregulation. Our findings demonstrate that both systemic and somatic disruption of circadian rhythms contribute to cancer progression.
Address David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA; Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. Electronic address: tjacks@mit.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 1550-4131 ISBN Medium
Area Expedition Conference
Notes PMID:27476975 Approved no
Call Number LoNNe @ kyba @ Serial 1497
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