Neuronal Apoptosis and Necrosis Following Spinal Cord Ischemia in the Rat

Kato, Hiroyuki; Kanellopoulos, Georgios K.; Matsuo, Sadashige; Wu, Ying; Jacquin, Mark F.; Hsu, Chung Y.; Kouchoukos, Nicholas T.; Choi, Dennis W.

doi:10.1006/exnr.1997.6707

Cited by 92 publications

(59 citation statements)

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“…[29][30][31][32][33] Although necrosis is considered characteristic of secondary cell death, studies have revealed that much of the neuronal and glial cell loss after injury results from apoptosis. [29][30][31][32] Apoptotic death of oligodendrocytes has been observed along the longitudinal axis of the spinal cord, and this may be involved in prolonged demyelination and deterioration of sensorimotor function. 33 Interventions that target apoptosis may therefore be beneEcial for the prevention of secondary degeneration following traumatic SCI.…”

Section: Discussionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor-γ agonist rosiglitazone reduces secondary damage in experimental spinal cord injury

et al. 2013

J Int Med Res

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Objective: To investigate the neuroprotective effects of rosiglitazone in a rat traumatic spinal cord injury (SCI) model. Methods: Adult Sprague-Dawley rats (n ¼ 12/group) underwent laminectomy (sham), SCI, SCI and rosiglitazone treatment (2 mg/kg twice daily for 7 days), or SCI and saline injection (vehicle). SCI was induced via dural application of an aneurysm clip. Spinal cord apoptosis and levels of tumour necrosis factor-a (TNFa), interleukin (IL)-1b, myeloperoxidase (MPO) and the apoptosisassociated proteins B-cell leukaemia/lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were examined 24 h after SCI. Locomotor function was evaluated 3, 7, 10, 14 and 21 days after SCI. Results: At 24 h after SCI, apoptosis and TNFa, IL-1b and MPO concentrations were significantly lower in the rosiglitazone group than in the vehicle and SCI groups. SCI resulted in an increase in Bax and a decrease in Bcl-2, which was reversed by rosiglitazone treatment. Rats in the rosiglitazone group had significantly better functional recovery than those in the vehicle and SCI groups. Conclusion: Rosiglitazone signiEcantly improved functional recovery, probably via attenuation of the local inflammatory reaction and reduced apoptosis.

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Section: Discussionmentioning

confidence: 99%

Peroxisome proliferator-activated receptor-γ agonist rosiglitazone reduces secondary damage in experimental spinal cord injury

et al. 2013

J Int Med Res

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“…Apoptosis is defined as programmed cell death, recognised following ischemic and traumatic injury to the CNS [72,[79][80][81] . Decreased perfusion and subsequent ischemia may be important pro-apoptotic events in cervical myelopathy, given the hypersensitivity of neurons and oligodendrocytes to ischaemic injury.…”

Section: Apoptosismentioning

confidence: 99%

Mechanical and cellular processes driving cervical myelopathy

Dolan

Butler

O’Byrne

et al. 2016

WJO

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Cervical myelopathy is a well-described clinical syndrome that may evolve from a combination of etiological mechanisms. It is traditionally classified by cervical spinal cord and/or nerve root compression which varies in severity and number of levels involved. The vast array of clinical manifestations of cervical myelopathy cannot fully be explained by the simple concept that a narrowed spinal canal causes compression of the cord, local tissue ischemia, injury and neurological impairment. Despite advances in surgical technology and treatment innovations, there are limited neuro-protective treatments for cervical myelopathy, which reflects an incomplete understanding of the pathophysiological processes involved in this disease. The aim of this review is to provide a comprehensive overview of the key pathophysiological processes at play in the development of cervical myelopathy.

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“…Caspases, formerly known as cysteine proteases, are the key regulators of apoptosis. [4][5][6][7] Various caspases and apoptotic cascades induced by caspase-dependent signaling have been described. There are several studies demonstrating promising results for preventing secondary injury in SCI with inhibition of apoptosis.…”

Section: Sonuçmentioning

confidence: 99%