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 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.

• Authors: Z-Y Zhang, Z Zhang, U Fauser, M Artelt, M Burnet, H J Schluesener
• Journal: Neuroscience (Neuroscience) Vol. 147 Issue 3 Pg. 720-6 (Jul 13 2007) ISSN: 0306-4522 [Print] United States
• PMID: 17560042 (Publication Type: Journal Article)

Chemical References

• Anti-Inflammatory Agents
• Col23a1 protein, rat
• Endostatins
• Dexamethasone
• Collagen

Topics

• Animals
• Anti-Inflammatory Agents (administration & dosage)
• Brain Injuries (drug therapy, metabolism)
• Cell Count
• Collagen (metabolism)
• Dexamethasone (administration & dosage)
• Endostatins (metabolism)
• Male
• Rats
• Rats, Inbred Lew
• Time Factors
• Up-Regulation (drug effects)