Endothelial cell loss is not a major cause of neuronal and glial cell death following contusion injury of the spinal cord

被引:64
作者
Casella, Gizelda T. B.
Bunge, Mary Bartlett
Wood, Patrick M.
机构
[1] Univ Miami, Sch Med, Miami Project Cure Paralysis, Miami, FL 33136 USA
[2] Univ Miami, Sch Med, Dept Cell Biol, Miami, FL 33136 USA
[3] Univ Miami, Sch Med, Dept Anat, Miami, FL 33136 USA
[4] Univ Miami, Sch Med, Dept Neurol Surg, Miami, FL 33136 USA
关键词
activated macrophage; apoptosis; microglia; necrosis; secondary injury;
D O I
10.1016/j.expneurol.2006.05.028
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 X 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. (c) 2006 Elsevier Inc. All rights reserved.
引用
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页码:8 / 20
页数:13
相关论文
共 78 条
[61]   Reduction of lipofuscin-like autofluorescence in fluorescently labeled tissue [J].
Schnell, SA ;
Staines, WA ;
Wessendorf, MW .
JOURNAL OF HISTOCHEMISTRY & CYTOCHEMISTRY, 1999, 47 (06) :719-730
[62]  
SCHUGER L, 1989, LAB INVEST, V61, P62
[63]  
SEARLE J, 1982, PATHOL ANNU, V17, P229
[64]   Expression of capillary basement membrane components during sequential phases of wound angiogenesis [J].
Sephel, GC ;
Kennedy, R ;
Kudravi, S .
MATRIX BIOLOGY, 1996, 15 (04) :263-279
[65]  
Shuman SL, 1997, J NEUROSCI RES, V50, P798, DOI 10.1002/(SICI)1097-4547(19971201)50:5<798::AID-JNR16>3.3.CO
[66]  
2-#
[67]   Activation of the caspase-3 apoptotic cascade in traumatic spinal cord injury [J].
Springer J.E. ;
Azbill R.D. ;
Knapp P.E. .
Nature Medicine, 1999, 5 (8) :943-946
[68]   Cytokine mRNA profiles in contused spinal cord and axotomized facial nucleus suggest a beneficial role for inflammation and gliosis [J].
Streit, WJ ;
Semple-Rowland, SL ;
Hurley, SD ;
Miller, RC ;
Popovich, PG ;
Stokes, BT .
EXPERIMENTAL NEUROLOGY, 1998, 152 (01) :74-87
[69]   Anoxic and ischemic injury of myelinated axons in CNS white matter: From mechanistic concepts to therapeutics [J].
Stys, PK .
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM, 1998, 18 (01) :2-25
[70]   Role of neutrophils in spinal cord injury in the rat [J].
Taoka, Y ;
Okajima, K ;
Uchiba, M ;
Murakami, K ;
Kushimoto, S ;
Johno, M ;
Naruo, M ;
Okabe, H ;
Takatsuki, K .
NEUROSCIENCE, 1997, 79 (04) :1177-1182