In Vivo Bcl-2 Oncogene Neuronal Expression in the Rat Spinal Cord

Lou, Jueren; Lenke, Lawrence G.; Xu, Fang; O’Brien, Michael F.

doi:10.1097/00007632-199803010-00001

Cited by 29 publications

(14 citation statements)

References 31 publications

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“…This finding is in agreement with previous studies demonstrating that acupuncture could repress apoptosis and promotes functional recovery after SCI [33,35,41]. Motoyama et al confirmed that neurons died in great quantities in Bcl-2-deficient gene mice [16], while more nerve tissues got protection in spinal cords of transferred Bcl-2 gene rats [42]. In contrast, Bax plays a crucial role in promoting cell apoptosis [43] and downregulation of Bax markedly reduces programmed cell death in the Bax knocked-out mice [17,18].…”

Section: The Effects Of Ea On Bax and Bcl-2 Expressionsupporting

confidence: 91%

Electro-acupuncture Reduces Neuronal Apoptosis Linked to Bax and Bcl-2 Expression in the Spinal Cords of Cats Subjected to Partial Dorsal Root Ganglionectomy

Zhao

Liu

et al. 2008

Neurochem Res

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While electro-acupuncture (EA) has been well known to contribute towards neuroplasticity occurring in both the central and the peripheral nervous system after injury, the underlying mechanism remains largely unknown. This study evaluated the effects and the possible mechanism of EA on neuronal apoptosis in the spinal cords of cats subjected to the removal of L(1)-L(5) and L(7)-S(2) dorsal root ganglion, sparing the L(6) dorsal root ganglion. EA treatment decreased the number of TUNEL-positive apoptotic cells in lamina II of the L(3) and L(6) cord segments at 7 and 14 days post operation (dpo). This EA-mediated neuroprotection is associated with a decrease in the number of Bax immunoreactive neurons and an increase in the number of Bcl-2 immunoreactive neurons. Furthermore, Western blot and RT-PCR analysis revealed a significant downregulation of Bax protein and its mRNA, but an upregulation of Bcl-2 in the dorsal horn of L(3) and L(6) cords at both 7 and 14 dpo. The present findings suggest that EA could inhibit neuronal apoptosis in dorsal root deafferentated cat spinal cords, possibly by Bax downregulation and Bcl-2 upregulation.

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Section: The Effects Of Ea On Bax and Bcl-2 Expressionsupporting

confidence: 91%

Electro-acupuncture Reduces Neuronal Apoptosis Linked to Bax and Bcl-2 Expression in the Spinal Cords of Cats Subjected to Partial Dorsal Root Ganglionectomy

Zhao

Liu

et al. 2008

Neurochem Res

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“…19,23 One such anti-apoptotic agent, the oncogene Bcl-2, has already been shown to improve histologic survival following an acute experimental spinal cord injury in the rat model. 24 Bcl-2 overexpression was produced invivo following introduction of the Bcl-2 gene via a recombinant adenovirus vector prior to the same experimental spinal cord injury administered in this study. Bcl-2 appears to inhibit apoptotic cell death by regulating an antioxidant pathway that limits free radical generation.…”

Section: Discussionmentioning

confidence: 99%

Apoptosis as a mechanism of neuronal cell death following acute experimental spinal cord injury

et al. 1998

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“…These responses to injury are likely to be mediated and reflected by changes in mRNA concentrations, regardless of whether these changes are due to regulated gene expression or to altered cellular populations. Many investigators have measured the expression of individual genes in injured spinal cords, particularly genes involved with inflammation (1,21,34,42,45,49,52,53), apoptosis (11,33,39,41), excitotoxicity (19,20), and neurotrophin stimulation (21,29,41). None, however, has measured large numbers of genes and their temporal and spatial relationships.…”

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confidence: 99%

Gene expression profiling of acute spinal cord injury reveals spreading inflammatory signals and neuron loss

Carmel

Galante²,

Soteropoulos³

et al. 2001

Physiological Genomics

141

113

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We have completed the first large-scale gene expression study of acute spinal cord injury (SCI) in rat. Oligonucleotide microarrays containing 1,200 gene-specific probes were used to quantify mRNA levels, relative to uninjured controls, in spinal cords injured using a standard contusion model. Our results revealed a marked loss of neuron-specific mRNAs at the injury site. The surviving cells showed a characteristic inflammatory response that started at the injury site and spread to the distal cord. Changes in several mRNA levels were associated with putative regenerative responses in the spinal cord. Notably, phosphodiesterase 4, nestin, glia-derived neurite promoting factor, and GAP-43 mRNAs increased significantly. Other mRNAs clustered temporally and spatially with these regeneration-associated genes. Thus we have described global patterns of gene expression following acute SCI, and we have identified targets for future study and possible therapeutic intervention.

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In Vivo Bcl-2 Oncogene Neuronal Expression in the Rat Spinal Cord

Cited by 29 publications

References 31 publications

Electro-acupuncture Reduces Neuronal Apoptosis Linked to Bax and Bcl-2 Expression in the Spinal Cords of Cats Subjected to Partial Dorsal Root Ganglionectomy

Electro-acupuncture Reduces Neuronal Apoptosis Linked to Bax and Bcl-2 Expression in the Spinal Cords of Cats Subjected to Partial Dorsal Root Ganglionectomy

Apoptosis as a mechanism of neuronal cell death following acute experimental spinal cord injury

Gene expression profiling of acute spinal cord injury reveals spreading inflammatory signals and neuron loss

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