TY - JOUR
T1 - Endothelial cell loss is not a major cause of neuronal and glial cell death following contusion injury of the spinal cord
AU - Casella, Gizelda T.B.
AU - Bunge, Mary Bartlett
AU - Wood, Patrick M.
N1 - Funding Information:
We thank Drs. Alex Marcillo and Youichi Yanagawa for performing weight drop injuries, Susan Kraydieh for the assistance with histological preparations, Andrew Weber for perfusing the animals, and Dr. Robert Duncan (Department of Epidemiology and Public Health, University of Miami School of Medicine) for the assistance with the statistical analysis of the data. This work was supported by the Miami Project to Cure Paralysis and NINDS NS 38665. GTBC was a Lois Pope LIFE Fellow.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2006/11
Y1 - 2006/11
N2 - Contusion of the spinal cord causes an immediate local loss of neurons and disruption of vasculature; additional loss continues thereafter. To explore the possibility of a causal link between delayed endothelial cell (EC) death and secondary neural cell loss, we evaluated neural and endothelial cell survival, and measured inflammatory cell infiltration, at times up to 48 h after contusion injury to the adult rat thoracic spinal cord. Female Fischer rats (200 g), subjected to moderate (10 g × 12.5 mm) weight drop injuries by the MASCIS (NYU) impactor, were analyzed at 15 min and at 1, 8, 24 and 48 h. ECs, neurons, astrocytes, oligodendrocytes, neutrophils and activated macrophages/microglia were counted in transverse sections. At the injury site, 90% of all neurons died within 48 h of injury; no medium-large diameter neurons survived beyond 48 h. EC death occurred with kinetics similar to glial cell death. Because, in the injury site, most cell death occurred before 8 h, it preceded inflammatory cell infiltration. Three millimeters rostral and caudal to the injury epicenter neuronal numbers were stable for 8 h, and a sharp decrease in neuronal numbers beginning at 8 h strongly correlated with the onset of inflammatory cell infiltration. Glial and blood vessel numbers remained relatively stable in these areas up to 48 h. These results suggest that the loss of ECs during the first 48 h after a contusion injury is not a major cause of neuronal and glial cell death and, in tissue adjacent to the epicenter, inflammatory cell infiltration leads to neuronal loss.
AB - Contusion of the spinal cord causes an immediate local loss of neurons and disruption of vasculature; additional loss continues thereafter. To explore the possibility of a causal link between delayed endothelial cell (EC) death and secondary neural cell loss, we evaluated neural and endothelial cell survival, and measured inflammatory cell infiltration, at times up to 48 h after contusion injury to the adult rat thoracic spinal cord. Female Fischer rats (200 g), subjected to moderate (10 g × 12.5 mm) weight drop injuries by the MASCIS (NYU) impactor, were analyzed at 15 min and at 1, 8, 24 and 48 h. ECs, neurons, astrocytes, oligodendrocytes, neutrophils and activated macrophages/microglia were counted in transverse sections. At the injury site, 90% of all neurons died within 48 h of injury; no medium-large diameter neurons survived beyond 48 h. EC death occurred with kinetics similar to glial cell death. Because, in the injury site, most cell death occurred before 8 h, it preceded inflammatory cell infiltration. Three millimeters rostral and caudal to the injury epicenter neuronal numbers were stable for 8 h, and a sharp decrease in neuronal numbers beginning at 8 h strongly correlated with the onset of inflammatory cell infiltration. Glial and blood vessel numbers remained relatively stable in these areas up to 48 h. These results suggest that the loss of ECs during the first 48 h after a contusion injury is not a major cause of neuronal and glial cell death and, in tissue adjacent to the epicenter, inflammatory cell infiltration leads to neuronal loss.
KW - Activated macrophage
KW - Apoptosis
KW - Microglia
KW - Necrosis
KW - Secondary injury
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U2 - 10.1016/j.expneurol.2006.05.028
DO - 10.1016/j.expneurol.2006.05.028
M3 - Article
C2 - 16872600
AN - SCOPUS:33748429148
VL - 202
SP - 8
EP - 20
JO - Experimental Neurology
JF - Experimental Neurology
SN - 0014-4886
IS - 1
ER -