Apoptosis and Expression of Bcl-2 after Compression Trauma to Rat Spinal Cord

Li, Gui Lin; Brodin, Greger; Farooque, M.; Funa, Keiko; Holtz, Anders; Wang, Wen Liang; Olsson, Yngve

doi:10.1097/00005072-199603000-00003

Cited by 238 publications

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“…Apoptosis after SCI has been confirmed by many groups including ours. 16,29,30 Pre-treatment of neurons in vitro with 17b-estradiol increased bcl-2 levels and enhanced the survival of neurons from excitotoxicity. 31 Moreover, after brain ischemia the bcl-2 signal was higher in females compared to males in the ischemic penumbra.…”

Section: Discussionmentioning

confidence: 99%

“…10 We have been using a compression SCI model to study the pathophysiology of primary and secondary injury. [11][12][13][14][15][16] Previously, we have shown that in this model there is a necrotizing lesion at the site of compression after moderate injury, which causes atrophy of the spinal cord at 14 days postinjury. 17 Morphometry of hematoxylin and eosin (H&E) and luxol fast blue (LFB)-stained sections as well as microtubule-associated protein 2 (MAP-2) immunocytochemical staining showed that both gray and white matter were reduced.…”

Section: Introductionmentioning

confidence: 86%

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Gender-related differences in recovery of locomotor function after spinal cord injury in mice

Farooque

Suo

et al. 2005

Spinal Cord

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Study design: In order to study the role of gender in recovery, we induced a thoracic compression spinal cord injury (SCI) separately in 2-month-old male and female C57Bl/6 mice. Objectives: We intended to assess effects of gender on recovery of hindlimb motor function and to correlate these with histomorphologic profiles of injured spinal cord tissue. Methods: Locomotor function was evaluated by three means: a modified locomotor scoring system for rodents, beam walking and computerized activity meter. Histology was analyzed by comparison of hematoxylin and eosin-stained perfused specimens. Results: Locomotor scores were 2.270.9 on day 1 in male mice, while, in contrast, they were significantly higher, 7.371.7, in females (Po0.02). On day 14 Basso, Beattie and Bresnahan scores were 9.572.2 in male mice and 16.072.2 in females (Po0.03). Terminal histology showed that the spinal cord architecture was relatively better preserved in female mice and that the extent of necrosis and infiltration of inflammatory cells was less compared to males. Setting: Neurobiology Research Laboratory of University of Kansas Medical School in US Department of Veterans Affairs Medical Center, Kansas City, Missouri. Conclusion: We found that the severity of the initial injury as well as the ultimate recovery of motor function after SCI is significantly influenced by gender, being remarkably better in females. The mechanism(s) of neuroprotection in females, although not yet elucidated, may be associated with the effects of estrogen on pathophysiological processes (blood flow, leukocyte migration inhibition, antioxidant properties, and inhibition of apoptosis).

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 86%

Gender-related differences in recovery of locomotor function after spinal cord injury in mice

Farooque

Suo

et al. 2005

Spinal Cord

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“…A number of studies have provided compelling evidence of widespread apoptosis of neurons, oligodendroglia, and microglia following SCI (Katoh et al, 1996;Li et al, 1996;Crowe et al, 1997;Shuman et al, 1997;Emery et al, 1998;Hayashi et al, 1998;Lou et al, 1998;Yong et al, 1998). An excellent review by Beattie et al provides a summary of current findings (Beattie et al, 2000).…”

Section: Traumatic Spinal Cord Injurymentioning

confidence: 99%

Apoptotic Cell Death Following Traumatic Injury to the Central Nervous System

Springer¹

2002

BMB Reports

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Apoptotic cell death is a fundamental and highly regulated biological process in which a cell is instructed to actively participate in its own demise. This process of cellular suicide is activated by developmental and environmental cues and normally plays an essential role in eliminating superfluous, damaged, and senescent cells of many tissue types. In recent years, a number of experimental studies have provided evidence of widespread neuronal and glial apoptosis following injury to the central nervous system (CNS). These studies indicate that injury-induced apoptosis can be detected from hours to days following injury and may contribute to neurological dysfunction. Given these findings, understanding the biochemical signaling events controlling apoptosis is a first step towards developing therapeutic agents that target this cell death process. This review will focus on molecular cell death pathways that are responsible for generating the apoptotic phenotype. It will also summarize what is currently known about the apoptotic signals that are activated in the injured CNS, and what potential strategies might be pursued to reduce this cell death process as a means to promote functional recovery.

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“…8,9 Depending on the severity of injury, post-SCI apoptosis affects a much greater extent of area than primary injury. 10 In addition, similar to the phenomenon in brain, apoptotic cell death could occur and progress even a few days after the onset of ischemia.…”

Section: Introductionmentioning

confidence: 99%

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

et al. 2004

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Study design: A standardized animal model of contusive spinal cord injury (SCI) with incomplete paraplegia was used to test the hypothesis that moderate systemic hypothermia reduces neural cell death. Terminal deoxynucleotidyl transferase [TdT]-mediated deoxyuridine triphosphate [dUTP] nick-end labeling (TUNEL) staining was used as a marker of apoptosis or cell damage. Objective: To determine whether or not moderate hypothermia could have a neuroprotective effect in neural cell death following spinal cord injury in rats. Setting: Kagawa Medical University, Japan. Methods: Male Sprague-Dawley (SD) rats (n ¼ 39) weighing on average 300 g (280-320 g) were used to prepare SCI models. After receiving contusive injury at T11/12, rats were killed at 24 h, 72 h, or 7 days after injury. The spinal cord was removed en bloc and of examined at five segments: 5 and 10 mm rostral to the center of injury, center of injury, and 5 and 10 mm caudal to the center of injury. Rats that received hypothermia (321C/4 h) were killed at the same time points as those that received normothermia (371C/3 h). The specimens were stained with hematoxylin and eosin, and subjected to in situ nick-end labeling (TUNEL), a specific method for visualizing cell death in the spinal cord. Results: At 24 h postinjury, TUNEL positive cells (TPC) decreased significantly 10 mm rostral to center of injury in hypothermic animals compared to the normothermia group. At 72 h post-SCI, TPC also decreased significantly at 5 mm rostral, and 5 and 10 mm caudal to the lesion center compared to normothermic animals. At 7 days postinjury, a significant decrease of TPC was observed at the 5 mm rostral and 5 mm caudal sites compared to normothermic animals. Conclusion: These results indicate that systemic hypothermia has a neuroprotective effect following SCI by attenuating post-traumatic TPC.

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Apoptosis and Expression of Bcl-2 after Compression Trauma to Rat Spinal Cord

Cited by 238 publications

References 0 publications

Gender-related differences in recovery of locomotor function after spinal cord injury in mice

Gender-related differences in recovery of locomotor function after spinal cord injury in mice

Apoptotic Cell Death Following Traumatic Injury to the Central Nervous System

Post-traumatic moderate systemic hypothermia reduces TUNEL positive cells following spinal cord injury in rat

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