Lesional expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following traumatic brain injury (TBI)

• Published in: Experimental neurology Vol. 208; no. 2; pp. 228 - 237
• Main Authors: Mueller, C.A., Schluesener, H.J., Fauser, U., Conrad, S., Schwab, J.M.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Inc 01.12.2007; Elsevier
• Subjects: Angiogenesis Inhibitors - metabolism; Animals; Antiangiogenesis; Biological and medical sciences; Blood Vessels - physiopathology; Brain - blood supply; Brain - metabolism; Brain - pathology; Brain Injuries - metabolism; Brain Injuries - pathology; Brain Injuries - physiopathology; CNS injury; Collagen Type XVIII - metabolism; Endostatins - metabolism; Injuries of the nervous system and the skull. Diseases due to physical agents; Macrophages - metabolism; Macrophages - pathology; Male; Medical sciences; Microglia - metabolism; Microglia - pathology; Necrosis; Neurology; Rats; Rats, Sprague-Dawley; Tissue Distribution; Traumas. Diseases due to physical agents; Vascular remodelling; Wounds, Stab - metabolism; Wounds, Stab - pathology; Wounds, Stab - physiopathology; Antiangiogenesis; Vascular remodelling; CNS injury; Angiogenesis; Nervous system diseases; Collagen; Glycoprotein; Central nervous system; Head trauma
• ISSN: 0014-4886; 1090-2430
• DOI: 10.1016/j.expneurol.2007.07.020

We have analysed the expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following stab wound injury and observed a highly significant ( p < 0.0001) lesional accumulation confined to areas of pan-necrotic injury and developing secondary damage. Maximal cell numbers were detected at Day 14, declining until Day 21 after injury. Further, endostatin/collagen XVIII + monocytic cells accumulated in Virchow–Robin spaces where they formed cell clusters. Besides being prevailingly localised to ED1 + activated microglia/macrophages, endostatin/collagen XVIII expression was also detected by subendothelial surrounding vessels in the lesioned area. Late and prolonged accumulation of endostatin/collagen XVIII + microglia/macrophages and increased numbers of endostatin/collagen XVIII + subendothelial cells/vessels in areas of vascular pruning and regression, point to a role in the termination of the transient angiogenic response, linked to a “late” inflammatory milieu.