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  • 1
    Electronic Resource
    Electronic Resource
    N-cadherin expression in endothelial cells during early angiogenesis in the eye and brain of the chicken: relation to blood–retina and blood–brain barrier development* (1999)
    Oxford, UK : Blackwell Science Ltd
    European journal of neuroscience 11 (1999), S. 0 
    Details
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The factors responsible for the induction and maintenance of blood–brain barrier properties are still undefined. The process of blood–brain barrier formation is thought to take place in a two-stage manner: the initial commitment of vascular sprouts by neuroectodermal cells may be followed by the stabilization of barrier properties. In the present study, we investigated the expression pattern of neural (N)-cadherin during early angiogenesis in the brain and the pecten oculi of the chicken. The pecten has been introduced previously as a model for the investigation of the formation and maturation of barrier properties in the central nervous system. Whereas perineural and choroid vessels remained immunonegative for N-cadherin, vascular sprouts invading both the brain and the pecten primordium acquired anti-N-cadherin immunoreactivity. Confocal laser scanning and immunoelectron microscopy indicated that the antigen was located at the ablumenal endothelial membrane in contact with subendothelial cells. With the onset of barrier differentiation as determined by junctional restriction of the tight junction protein occludin, N-cadherin labelling rapidly decreased. Specific intraneuroectodermal upregulation and decline of endothelial N-cadherin was confirmed by in situ hybridization and suggests that N-cadherin expression by cerebral and pecteneal endothelial cells represents an initial and transient signal which may be involved in the commitment of early blood vessels to express blood–brain and blood–retina barrier properties.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1460-9568.1999.00526.x
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Claudin-1 and claudin-5 expression and tight junction morphology are altered in blood vessels of human glioblastoma multiforme (2000)
    Springer
    Acta neuropathologica 100 (2000), S. 323-331 
    Details
    ISSN: 1432-0533
    Keywords: Key words Glioma ; Blood-brain barrier ; Tight junction ; Claudin ; Pericytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the study was to characterize the interendothelial junctions in tumor microvessels of five cases of human glioblastoma multiforme. In addition to morphological analysis, tumors were screened for the expression of junctional proteins, such as occludin, claudin-1, ZO-1 and catenins. The expression of the tight junction protein claudin-1 was lost in the majority of tumor microvessels, whereas claudin-5 and occludin were significantly down-regulated only in hyperplastic vessels. As shown by freeze-fracture analysis, under the conditions of tumor growth tight junction particles of endothelial cells were almost exclusively associated with the exocytoplasmic fracture face, providing evidence for a switch of the particles from the protoplasmic to the external leaflet of the endothelial membrane. These results suggest a relationship between claudin-1 suppression and the alteration of tight junction morphology, which is likely to correlate with the increase of endothelial permeability. Underlining the undifferentiated state of tumor microvessels, plakoglobin, a crucial protein for mature endothelial junctions, was not detectable in most microvessels, whereas β-catenin was abundantly labeled. In this context, it is of particular interest that the majority of microvascular pericytes were negative for alpha-smooth muscle actin, which is a marker of differentiated pericytes, although pericytes were frequently found in electron micrographs. In conclusion, the data suggest that the increase in microvascular permeability in human gliomas, contributing to the clinically severe symptoms of brain edema, is a result of a dysregulation of junctional proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004010000180
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  • 3
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    Sonic hedgehog causes mural cells to jump 'n' run (2014)
    American Society of Hematology (ASH)
    In: Blood
    Details
    Publication Date: 2014-04-11
    Keywords: Free Research Articles
    Print ISSN: 0006-4971
    Electronic ISSN: 1528-0020
    Topics: Biology , Medicine
    Published by American Society of Hematology (ASH)
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  • 4
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    Soluble epoxide hydrolase and progenitor cells [Medical Sciences] (2012)
    National Academy of Sciences
    Details
    Publication Date: 2012-06-20
    Description: Fatty acid epoxides are important lipid signaling molecules involved in the regulation of vascular tone and homeostasis. Tissue and plasma levels of these mediators are determined by the activity of cytochrome P450 epoxygenases and the soluble epoxide hydrolase (sEH), and targeting the latter is an effective way of manipulating epoxide levels in vivo. We investigated the role of the sEH in regulating the mobilization and proliferation of progenitor cells with vasculogenic/reparative potential. Our studies revealed that sEH down-regulation/inhibition impaired the development of the caudal vein plexus in zebrafish, and decreased the numbers of lmo2/cmyb-positive progenitor cells therein. In mice sEH inactivation attenuated progenitor cell proliferation (spleen colony formation), but the sEH products 12,13-dihydroxyoctadecenoic acid (12,13-DiHOME) and 11,12- dihydroxyeicosatrienoic acid stimulated canonical Wnt signaling and rescued the effects of sEH inhibition. In murine bone marrow, the epoxide/diol content increased during G-CSF–induced progenitor cell expansion and mobilization, and both mobilization and spleen colony formation were reduced in sEH−/− mice. Similarly, sEH−/− mice showed impaired functional recovery following hindlimb ischemia, which was rescued following either the restoration of bone marrow sEH activity or treatment with 12,13-DiHOME. Thus, sEH activity is required for optimal progenitor cell proliferation, whereas long-term sEH inhibition is detrimental to progenitor cell proliferation, mobilization, and vascular repair.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 5
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    Acute myocardial infarction activates progenitor cells and increases Wnt signalling in the bone marrow (2012)
    Oxford University Press
    Details
    Publication Date: 2012-08-02
    Description: Aims We aimed to characterize the influence of acute myocardial infarction (AMI) on the metabolic activity of the bone marrow (BM) and on the composition and functional activity of BM-derived mononuclear cells (BMC). Acute ischaemia or other stressors induce the mobilization of progenitor cells from the BM stem cell niche. The effect of AMI on the numbers and functional activity of cells within the BM is unknown. Methods and results In patients of the REPAIR-AMI trial as well as in mice, the number and functionality of BMC was compared with respect to the time interval from AMI. Activation of Wnt signalling was assessed after AMI induction in TOP-GAL transgenic reporter mice, carrying a β-galactosidase gene driven by an LEF/TCF/β-catenin responsive promoter. The metabolic activity of the BM, as determined by F-18-fluorodeoxyglucose-positron emission tomography, was significantly higher in patients with AMI compared with patients with chronic post-ischaemic heart failure. Moreover, the number of haematopoietic CD34 + ( P 〈 0.05) and CD133 + ( P 〈 0.05) cells in the BM aspirates was significantly increased in patients within 7 days after AMI. In order to confirm these clinical data, we induced AMI in mice, which time-dependently increased the number of c-kit + Sca-1 + lin- cells and colony-forming units in the BM. Activation of the BM by AMI induced a significant increase in Wnt signalling, which is known to induce proliferation of haematopoietic stem cells, and demonstrated increased levels of the Wnt target Axin-2 in BM-derived cells on Day 7 ( P 〈 0.01 vs. control). Conclusion Acute myocardial infarction is associated with an increased metabolic activity and increased levels of progenitor cells within days after AMI. These findings document an activation of the stem cell niche within the BM following AMI, which may have important implications for the optimal timing of cell aspirations used for therapeutic application in patients with AMI.
    Print ISSN: 0195-668X
    Electronic ISSN: 1522-9645
    Topics: Medicine
    Published by Oxford University Press
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  • 6
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    Endothelial Wnt/{beta}-catenin signaling inhibits glioma angiogenesis and normalizes tumor blood vessels by inducing PDGF-B expression (2012)
    Rockefeller University Press
    Details
    Publication Date: 2012-08-28
    Description: Endothelial Wnt/β-catenin signaling is necessary for angiogenesis of the central nervous system and blood–brain barrier (BBB) differentiation, but its relevance for glioma vascularization is unknown. In this study, we show that doxycycline-dependent Wnt1 expression in subcutaneous and intracranial mouse glioma models induced endothelial Wnt/β-catenin signaling and led to diminished tumor growth, reduced vascular density, and normalized vessels with increased mural cell attachment. These findings were corroborated in GL261 glioma cells intracranially transplanted in mice expressing dominant-active β-catenin specifically in the endothelium. Enforced endothelial β-catenin signaling restored BBB characteristics, whereas inhibition by Dkk1 (Dickkopf-1) had opposing effects. By overactivating the Wnt pathway, we induced the Wnt/β-catenin–Dll4/Notch signaling cascade in tumor endothelia, blocking an angiogenic and favoring a quiescent vascular phenotype, indicated by induction of stalk cell genes. We show that β-catenin transcriptional activity directly regulated endothelial expression of platelet-derived growth factor B (PDGF-B), leading to mural cell recruitment thereby contributing to vascular quiescence and barrier function. We propose that reinforced Wnt/β-catenin signaling leads to inhibition of angiogenesis with normalized and less permeable vessels, which might prove to be a valuable therapeutic target for antiangiogenic and edema glioma therapy.
    Print ISSN: 0022-1007
    Electronic ISSN: 1540-9538
    Topics: Medicine
    Published by Rockefeller University Press
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  • 7
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    Environmental Transcription of mmoX by Methane-Oxidizing Proteobacteria in a Subarctic Palsa Peatland [Environmental Microbiology] (2012)
    The American Society for Microbiology (ASM)
    Details
    Publication Date: 2012-12-29
    Description: Methane-oxidizing bacteria (MOB) that possess the soluble form of methane monooxygenase (sMMO) are present in various environments, but unlike the prevalent particulate methane monooxygenase (pMMO), the in situ activity of sMMO has not been documented. Here we report on the environmental transcription of a gene ( mmoX ) for this enzyme, which was attributed mainly to MOB lacking a pMMO. Our study indicates that the sMMO is an active enzyme in acidic peat ecosystems, but its importance for the mitigation of methane releases remains unknown.
    Print ISSN: 0099-2240
    Electronic ISSN: 1098-5336
    Topics: Biology
    Published by The American Society for Microbiology (ASM)
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  • 8
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    Nucleoside Diphosphate Kinase B Regulates Angiogenesis Through Modulation of Vascular Endothelial Growth Factor Receptor Type 2 and Endothelial Adherens Junction Proteins [Basic Sciences] (2014)
    American Heart Association (AHA)
    Details
    Publication Date: 2014-09-18
    Description: Objective— Nucleoside diphosphate kinase B (NDPKB) participates in the activation of heterotrimeric and monomeric G proteins, which are pivotal mediators in angiogenic signaling. The role of NDPKB in angiogenesis has to date not been defined. Therefore, we analyzed the contribution of NDPKB to angiogenesis and its underlying mechanisms in well-characterized in vivo and in vitro models. Approach and Results— Zebrafish embryos were depleted of NDPKB by morpholino-mediated knockdown. These larvae displayed severe malformations specifically in vessels formed by angiogenesis. NDPKB-deficient (NDPKB –/– ) mice were subjected to oxygen-induced retinopathy. In this model, the number of preretinal neovascularizations in NDPKB –/– mice was strongly reduced in comparison with wild-type littermates. In accordance, a delayed blood flow recovery was detected in the NDPKB –/– mice after hindlimb ligation. In in vitro studies, a small interfering RNA–mediated knockdown of NDPKB was performed in human umbilical endothelial cells. NDPKB depletion impaired vascular endothelial growth factor (VEGF)–induced sprouting and hampered the VEGF-induced spatial redistributions of the VEGF receptor type 2 and VE-cadherin at the plasma membrane. Concomitantly, NDPKB depletion increased the permeability of the human umbilical endothelial cell monolayer. Conclusions— This is the first report to show that NDPKB is required for VEGF-induced angiogenesis and contributes to the correct localization of VEGF receptor type 2 and VE-cadherin at the endothelial adherens junctions. Therefore, our data identify NDPKB as a novel molecular target to modulate VEGF-dependent angiogenesis.
    Keywords: Angiogenesis, Animal models of human disease, Other Vascular biology
    Print ISSN: 1079-5642
    Electronic ISSN: 1524-4636
    Topics: Medicine
    Published by American Heart Association (AHA)
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  • 9
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    Methane turnover and methanotrophic communities in arctic aquatic ecosystems of the Lena Delta, Northeast Siberia (2016)
    Oxford University Press
    Details
    Publication Date: 2016-06-30
    Description: Large amounts of organic carbon are stored in Arctic permafrost environments, and microbial activity can potentially mineralize this carbon into methane, a potent greenhouse gas. In this study, we assessed the methane budget, the bacterial methane oxidation (MOX) and the underlying environmental controls of arctic lake systems, which represent substantial sources of methane. Five lake systems located on Samoylov Island (Lena Delta, Siberia) and the connected river sites were analyzed using radiotracers to estimate the MOX rates, and molecular biology methods to characterize the abundance and the community composition of methane-oxidizing bacteria (MOB). In contrast to the river, the lake systems had high variation in the methane concentrations, the abundance and composition of the MOB communities, and consequently, the MOX rates. The highest methane concentrations and the highest MOX rates were detected in the lake outlets and in a lake complex in a flood plain area. Though, in all aquatic systems, we detected both, Type I and II MOB, in lake systems, we observed a higher diversity including MOB, typical of the soil environments. The inoculation of soil MOB into the aquatic systems, resulting from permafrost thawing, might be an additional factor controlling the MOB community composition and potentially methanotrophic capacity.
    Print ISSN: 0168-6496
    Electronic ISSN: 1574-6941
    Topics: Biology
    Published by Oxford University Press
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  • 10
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    Sulfate deprivation triggers high methane production in a disturbed and rewetted coastal peatland (2019)
    In:  EPIC3Biogeosciences, 16(9), pp. 1937-1953
    Details
    Publication Date: 2020-11-17
    Repository Name: EPIC Alfred Wegener Institut
    Type: Article , isiRev
    Format: application/pdf
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