Dexamethasone transiently attenuates up-regulation of endostatin/collagen XVIII following traumatic brain injury

Abstract Endostatin/collagen XVIII is a specific inhibitor of endothelial proliferation and migration in vitro . It has also been shown to have anti-angiogenic activity and tumor growth inhibitory activity in vivo and in vitro . Here we studied expression of endostatin/collagen XVIII in a rat trauma...

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Bibliographic Details
Published in:Neuroscience 2007-07, Vol.147 (3), p.720-726
Main Authors: Zhang, Z.-Y, Zhang, Z, Fauser, U, Artelt, M, Burnet, M, Schluesener, H.J
Format: Article
Language:English
Subjects:
Animals
Anti-Inflammatory Agents - administration & dosage
Biological and medical sciences
Brain Injuries - drug therapy
Brain Injuries - metabolism
Cell Count
Collagen - metabolism
dexamethasone
Dexamethasone - administration & dosage
endostatin/collagen XVIII
Endostatins - metabolism
Fundamental and applied biological sciences. Psychology
Injuries of the nervous system and the skull. Diseases due to physical agents
Male
Medical sciences
microglia/macrophages
Neurology
Rats
Rats, Inbred Lew
Time Factors
Traumas. Diseases due to physical agents
traumatic brain injury
Up-Regulation - drug effects
Vertebrates: nervous system and sense organs
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Summary:Abstract Endostatin/collagen XVIII is a specific inhibitor of endothelial proliferation and migration in vitro . It has also been shown to have anti-angiogenic activity and tumor growth inhibitory activity in vivo and in vitro . Here we studied expression of endostatin/collagen XVIII in a rat traumatic brain injury (TBI) model, focusing on the early phase. A significant up-regulation of endostatin/collagen XVIII in TBI began as early as 24 h post-TBI. Double-staining experiment revealed that the major resource of endostatin/collagen XVIII+ cells in our TBI rat model was a subpopulation of reactivated microglia/macrophages. Our data further showed that dexamethasone attenuated up-regulation of endostatin/collagen XVIII expression at days 1 and 2, but not at day 4, post-TBI, indicating that dexamethasone might possess an early and transient influence to the angiogenesis following TBI.
ISSN:0306-4522
1873-7544
DOI:10.1016/j.neuroscience.2007.04.052