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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    New York, N.Y. : Wiley-Blackwell
    Journal of Cellular Biochemistry 52 (1993), S. 289-296 
    ISSN: 0730-2312
    Keywords: endothelium ; wound repair ; basic fibroblast growth factor ; suramin ; Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Monolayers of endothelial cells respond to physical denudation with a characteristic sequence of lamellipodia extrusion, cell migration, and cell proliferation. Basic fibroblast growth factor (bFGF) has been implicated as a necessary component of this process: addition of exogenous bFGF enhances monolayer regeneration both in vitro and in vivo, and monolayer regeneration can be inhibited in vitro by treatment with neutralizing antibodies raised against bFGF. Centrosome reorientation from a random location to one preferentially situated between the nucleus and the denudation edge has been postulated as a mechanism essential for cell polarization and subsequent migration. This present study examined the effects of a polyclonal antibody to bFGF and suramin on monolayer regeneration, actin microfilament staining, and centrosome orientation at the wound edge of partially denuded bovine large vessel endothelial monolayers. Treatment with anti-bFGF or suramin abolished monolayer repair in these cultures. Cells at the denudation edge showed altered actin staining patterns and reduced lamellipodia extrusion, and there was complete inhibition of centrosome reorientation in treated cultures. Monolayer repair and centrosome reorientation could be restored by addition of exogenous bFGF in antibody but not suramin treated cultures. Recent evidence suggests that preferential centrosome location in migrating cells may be a consequence of lamellipodia protrusion and cell spreading, rather than an indication of cell polarization. However, these results indicate that agents which interfere with bFGF availability prevent endothelial monolayer regeneration via mechanisms involving cell spreading and/or centrosome reorientation.
    Additional Material: 5 Ill.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0003-276X
    Keywords: Life and Medical Sciences ; Cell & Developmental Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Medicine
    Notes: In this study the three-dimensional organization of pinocytotic vesicles in mouse endothelia from permeable (choroid plexus, area postrema, and skeletal muscle) and blood-brain barrier (bbb) (cerebral gray and white matter) microvessels was examined. Reconstructions of 75 segments of endothelial cells from microvessels were done with very thin (〈23 nm) serial sections and tracings. A total of 2,013 vesicles from five tissues were reconstructed for this study. Vesicles were classified as to whether they were attached to other vesicles (fused), connected to golgi or endoplasmic peticulum (tubule-connected), open to vessel lumen or ablumen (surface-connected) or isolated in the cytoplasm (free).The densities of tubule-connected vesicles and free vesicles were the same in all four types of vessels. It seems unlikely, therefore, that these vesicles are related to vascular permeability. Vesicular clusters and surface-connected vesicles were found in much higher densities in area postrema, choroid plexus, and skeletal muscle vessels than in bbb vessels. Single-vesicle transendothelial channels were found in attenuated endothelia of area postrema and choroid plexus. These results support the hypothesis that endothelial vesicles play a role in vascular permeability, possibility by transient fusion of vesicle clusters to the plasmalemma, to form transendothelial channels.
    Additional Material: 3 Ill.
    Type of Medium: Electronic Resource
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