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  • 1
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    Acetylation-dependent regulation of endothelial Notch signalling by the SIRT1 deacetylase (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-04-19
    Description: Notch signalling is a key intercellular communication mechanism that is essential for cell specification and tissue patterning, and which coordinates critical steps of blood vessel growth. Although subtle alterations in Notch activity suffice to elicit profound differences in endothelial behaviour and blood vessel formation, little is known about the regulation and adaptation of endothelial Notch responses. Here we report that the NAD(+)-dependent deacetylase SIRT1 acts as an intrinsic negative modulator of Notch signalling in endothelial cells. We show that acetylation of the Notch1 intracellular domain (NICD) on conserved lysines controls the amplitude and duration of Notch responses by altering NICD protein turnover. SIRT1 associates with NICD and functions as a NICD deacetylase, which opposes the acetylation-induced NICD stabilization. Consequently, endothelial cells lacking SIRT1 activity are sensitized to Notch signalling, resulting in impaired growth, sprout elongation and enhanced Notch target gene expression in response to DLL4 stimulation, thereby promoting a non-sprouting, stalk-cell-like phenotype. In vivo, inactivation of Sirt1 in zebrafish and mice causes reduced vascular branching and density as a consequence of enhanced Notch signalling. Our findings identify reversible acetylation of the NICD as a molecular mechanism to adapt the dynamics of Notch signalling, and indicate that SIRT1 acts as rheostat to fine-tune endothelial Notch responses.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598045/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4598045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Guarani, Virginia -- Deflorian, Gianluca -- Franco, Claudio A -- Kruger, Marcus -- Phng, Li-Kun -- Bentley, Katie -- Toussaint, Louise -- Dequiedt, Franck -- Mostoslavsky, Raul -- Schmidt, Mirko H H -- Zimmermann, Barbara -- Brandes, Ralf P -- Mione, Marina -- Westphal, Christoph H -- Braun, Thomas -- Zeiher, Andreas M -- Gerhardt, Holger -- Dimmeler, Stefanie -- Potente, Michael -- R01 DK088190/DK/NIDDK NIH HHS/ -- R01 GM093072/GM/NIGMS NIH HHS/ -- R01DK088190-01A1/DK/NIDDK NIH HHS/ -- R01GM093072-01/GM/NIGMS NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2011 May 12;473(7346):234-8. doi: 10.1038/nature09917. Epub 2011 Apr 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe University, D-60590 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21499261" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Animals ; Endothelial Cells/cytology/*enzymology ; *Gene Expression Regulation ; Gene Knockout Techniques ; Gene Silencing ; HEK293 Cells ; Humans ; Mice ; Mutation ; Receptor, Notch1/metabolism ; Receptors, Notch/*metabolism ; Signal Transduction/*physiology ; Sirtuin 1/*genetics/*metabolism ; Zebrafish/embryology/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    FOXO1 couples metabolic activity and growth state in the vascular endothelium (2016)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2016-01-07
    Description: Endothelial cells (ECs) are plastic cells that can switch between growth states with different bioenergetic and biosynthetic requirements. Although quiescent in most healthy tissues, ECs divide and migrate rapidly upon proangiogenic stimulation. Adjusting endothelial metabolism to the growth state is central to normal vessel growth and function, yet it is poorly understood at the molecular level. Here we report that the forkhead box O (FOXO) transcription factor FOXO1 is an essential regulator of vascular growth that couples metabolic and proliferative activities in ECs. Endothelial-restricted deletion of FOXO1 in mice induces a profound increase in EC proliferation that interferes with coordinated sprouting, thereby causing hyperplasia and vessel enlargement. Conversely, forced expression of FOXO1 restricts vascular expansion and leads to vessel thinning and hypobranching. We find that FOXO1 acts as a gatekeeper of endothelial quiescence, which decelerates metabolic activity by reducing glycolysis and mitochondrial respiration. Mechanistically, FOXO1 suppresses signalling by MYC (also known as c-MYC), a powerful driver of anabolic metabolism and growth. MYC ablation impairs glycolysis, mitochondrial function and proliferation of ECs while its EC-specific overexpression fuels these processes. Moreover, restoration of MYC signalling in FOXO1-overexpressing endothelium normalizes metabolic activity and branching behaviour. Our findings identify FOXO1 as a critical rheostat of vascular expansion and define the FOXO1-MYC transcriptional network as a novel metabolic checkpoint during endothelial growth and proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wilhelm, Kerstin -- Happel, Katharina -- Eelen, Guy -- Schoors, Sandra -- Oellerich, Mark F -- Lim, Radiance -- Zimmermann, Barbara -- Aspalter, Irene M -- Franco, Claudio A -- Boettger, Thomas -- Braun, Thomas -- Fruttiger, Marcus -- Rajewsky, Klaus -- Keller, Charles -- Bruning, Jens C -- Gerhardt, Holger -- Carmeliet, Peter -- Potente, Michael -- K08CA090438/CA/NCI NIH HHS/ -- Cancer Research UK/United Kingdom -- England -- Nature. 2016 Jan 14;529(7585):216-20. doi: 10.1038/nature16498. Epub 2016 Jan 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Angiogenesis &Metabolism Laboratory, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, Department of Oncology, University of Leuven, Leuven 3000, Belgium. ; Laboratory of Angiogenesis and Neurovascular Link, Vesalius Research Center, VIB, Leuven 3000, Belgium. ; Vascular Biology Laboratory, London Research Institute, Cancer Research UK, London WC2A 3LY, UK. ; Vascular Morphogenesis Laboratory, Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon 1649-028, Portugal. ; Department of Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, D-61231 Bad Nauheim, Germany. ; UCL Institute of Ophthalmology, University College London, London EC1V 9EL, UK. ; Max Delbruck Center for Molecular Medicine (MDC), D-13125 Berlin, Germany. ; Children's Cancer Therapy Development Institute, Beaverton, Oregon 97005, USA. ; Max Planck Institute for Metabolism Research, Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Center of Molecular Medicine Cologne (CMMC), Center for Endocrinology, Diabetes and Preventive Medicine (CEDP), University of Cologne, D-50931 Cologne, Germany. ; Vascular Patterning Laboratory, Vesalius Research Center, VIB and University of Leuven, Leuven 3000, Belgium. ; DZHK (German Center for Cardiovascular Research), partner site Berlin, D-13347 Berlin, Germany. ; Berlin Institute of Health (BIH), D-10117 Berlin, Germany. ; International Institute of Molecular and Cell Biology, 02-109 Warsaw, Poland. ; DZHK (German Center for Cardiovascular Research), partner site Frankfurt Rhine-Main, D-13347 Berlin, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26735015" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Proliferation ; Cell Respiration ; Endothelium, Vascular/cytology/*growth & development/*metabolism ; Female ; Forkhead Transcription Factors/deficiency/genetics/*metabolism ; Glycolysis ; Human Umbilical Vein Endothelial Cells/cytology/metabolism ; Humans ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-myc/deficiency/genetics/metabolism ; Signal Transduction
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
    Electronic Resource
    Electronic Resource
    Non-newtonian behavior of suspensions (1980)
    Springer
    Acta mechanica 37 (1980), S. 85-97 
    Details
    ISSN: 1619-6937
    Source: Springer Online Journal Archives 1860-2000
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Description / Table of Contents: Zusammenfassung Es wird eine Theorie für nicht Newtonsches Verhalten von verdünnten Suspensionen gleichmäßig schwebender, starrer, kugeliger Teilchen in inkompressibler, Newtonscher Flüssigkeit hergeleitet. Es wird gezeigt, daß die Quelle nicht Newtonscher Effekte der Anteil der kinetischen Energie ist, der mit den Störungen in der Strömung zufolge der Anwesenheit der Teilchen verbunden ist. Es werden explizite Ausdrücke für die Stoffgleichungen der mittleren Spannung unter der Einschränkung langsam veränderlicher Strömungsbedingungen angegeben. Einflüsse der bezogenen Normalspannung werden in einigen Einzelheiten für den Fall der einfachen Scherströmung betrachtet.
    Notes: Summary A theory is derived for the non-Newtonian behavior of a dilute suspension of neutrally buoyant, rigid, spherical inclusions in an incompressible Newtonian fluid. The source of the non-Newtonian effects is shown to be that portion of the kinetic energy associated with the flow perturbation caused by the presence of the particles. Explicit forms are given for the average stress constitutive relation under the restriction of slowly varying flow conditions. Related normal stress effects are considered in some detail for the case of simple shearing flow.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01441246
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    Paper (German National Licenses)
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  • 4
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    Fault kinematics in northern Central America and coupling along the subduction interface of the Cocos Plate, from GPS data in Chiapas (Mexico), Guatemala and El Salvador (2012)
    Oxford University Press
    Details
    Publication Date: 2012-04-24
    Description: SUMMARY New GPS measurements in Chiapas (Mexico), Guatemala and El Salvador are used to constrain the fault kinematics in the North America (NA), Caribbean (CA) and Cocos (CO) plates triple junction area. The regional GPS velocity field is first analysed in terms of strain partitioning across the major volcano-tectonic structures, using elastic half-space modelling, then inverted through a block model. We show the dominant role of the Motagua Fault with respect to the Polochic Fault in the accommodation of the present-day deformation associated with the NA and CA relative motion. The NA/CA motion decreases from 18–22 mm yr −1 in eastern Guatemala to 14–20 mm yr −1 in central Guatemala (assuming a uniform locking depth of 14–28 km), down to a few millimetres per year in western Guatemala. As a consequence, the western tip of the CA Plate deforms internally, with ≃9 mm yr −1 of east–west extension (≃5 mm yr −1 across the Guatemala city graben alone). Up to 15 mm yr −1 of dextral motion can be accommodated across the volcanic arc in El Salvador and southeastern Guatemala. The arc seems to mark the northern boundary of an independent forearc sliver (AR), pinned to the NA plate. The inversion of the velocity field shows that a four-block (NA, CA, CO and AR) model, that combines relative block rotations with elastic deformation at the block boundaries, can account for most of the GPS observations and constrain the overall kinematics of the active structures. This regional modelling also evidences lateral variations of coupling at the CO subduction interface, with a fairly high-coupling (≃0.6) offshore Chiapas and low-coupling (≃0.25) offshore Guatemala and El Salvador.
    Print ISSN: 0956-540X
    Electronic ISSN: 1365-246X
    Topics: Geosciences
    Published by Oxford University Press on behalf of The Deutsche Geophysikalische Gesellschaft (DGG) and the Royal Astronomical Society (RAS).
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  • 5
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    Revisiting global fossil fuel and biofuel emissions of ethane (2017)
    Wiley
    Details
    Publication Date: 2017-02-09
    Description: Recent measurements over the Northern Hemisphere indicate that the long-term decline in the atmospheric burden of ethane (C 2 H 6 ) has ended, and the abundance increased dramatically between 2010 and 2014. The rise in C 2 H 6 atmospheric abundances has been attributed to oil and natural gas extraction in North America. Existing global C 2 H 6 emission inventories are based on outdated activity maps that do not account for current oil and natural gas exploitation regions. We present an updated global C 2 H 6 emission inventory based on 2010 satellite-derived CH 4 fluxes with adjusted C 2 H 6 emissions over the U.S. from the National Emission Inventory (NEI 2011). We contrast our global 2010 C 2 H 6 emission inventory with one developed for 2001. The C 2 H 6 difference between global anthropogenic emissions is subtle (7.9 versus 7.2 Tg yr −1 ), but the spatial distribution of the emissions is distinct. In the 2010 C 2 H 6 inventory, fossil fuel sources in the Northern Hemisphere represent half of global C 2 H 6 emissions and 95% of global fossil fuel emissions. Over the U.S., un-adjusted NEI 2011 C 2 H 6 emissions produce mixing ratios that are 14–50 % of those observed by aircraft observations (2008–2014). When the NEI 2011 C 2 H 6 emission totals are scaled by a factor of 1.4, the GEOS-Chem model largely reproduces a regional suite of observations, with the exception of the central U.S., where it continues to under-predict observed mixing ratios in the lower troposphere. We estimate monthly mean contributions of fossil fuel C 2 H 6 emissions to ozone and peroxyacetyl nitrate surface mixing ratios over North America of ~1% and ~8%, respectively.
    Print ISSN: 0148-0227
    Topics: Geosciences , Physics
    Published by Wiley on behalf of American Geophysical Union (AGU).
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  • 6
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    Non-newtonian behavior of suspensions (1980)
    Springer
    Details
    Publication Date: 1980-03-01
    Print ISSN: 0001-5970
    Electronic ISSN: 1619-6937
    Topics: Mechanical Engineering, Materials Science, Production Engineering, Mining and Metallurgy, Traffic Engineering, Precision Mechanics , Physics
    Published by Springer
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  • 7
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    Well-Defined, Model Long Chain Branched Polyethylene. 2. Melt Rheological Behavior (2002)
    American Chemical Society
    Details
    Publication Date: 2002-03-09
    Print ISSN: 0024-9297
    Electronic ISSN: 1520-5835
    Topics: Chemistry and Pharmacology , Physics
    Published by American Chemical Society
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