Lesional expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following traumatic brain injury (TBI)
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...
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Published in | Experimental neurology Vol. 208; no. 2; pp. 228 - 237 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier Inc
01.12.2007
Elsevier |
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Abstract | 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. |
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AbstractList | 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. 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. 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 super(+) monocytic cells accumulated in Virchow-Robin spaces where they formed cell clusters. Besides being prevailingly localised to ED1 super(+) 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 super(+) microglia/macrophages and increased numbers of endostatin/collagen XVIII super(+) 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. 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. |
Author | Conrad, S. Mueller, C.A. Fauser, U. Schwab, J.M. Schluesener, H.J. |
Author_xml | – sequence: 1 givenname: C.A. surname: Mueller fullname: Mueller, C.A. email: Christian-Andreas.Mueller@ukb.uni-bonn.de organization: Institute of Brain Research, Medical School, Eberhard-Karls University Tuebingen, Calwerstr. 3, 72076 Tuebingen, Germany – sequence: 2 givenname: H.J. surname: Schluesener fullname: Schluesener, H.J. organization: Institute of Brain Research, Medical School, Eberhard-Karls University Tuebingen, Calwerstr. 3, 72076 Tuebingen, Germany – sequence: 3 givenname: U. surname: Fauser fullname: Fauser, U. organization: Institute of Brain Research, Medical School, Eberhard-Karls University Tuebingen, Calwerstr. 3, 72076 Tuebingen, Germany – sequence: 4 givenname: S. surname: Conrad fullname: Conrad, S. organization: Institute of Brain Research, Medical School, Eberhard-Karls University Tuebingen, Calwerstr. 3, 72076 Tuebingen, Germany – sequence: 5 givenname: J.M. surname: Schwab fullname: Schwab, J.M. organization: Institute of Brain Research, Medical School, Eberhard-Karls University Tuebingen, Calwerstr. 3, 72076 Tuebingen, Germany |
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Keywords | Antiangiogenesis Vascular remodelling CNS injury Angiogenesis Nervous system diseases Collagen Glycoprotein Central nervous system Head trauma |
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SubjectTerms | 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 |
Title | Lesional expression of the endogenous angiogenesis inhibitor endostatin/collagen XVIII following traumatic brain injury (TBI) |
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