RGD Reference Report - Overexpression of SOD1 in transgenic rats attenuates nuclear translocation of endonuclease G and apoptosis after spinal cord injury. - Rat Genome Database

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Overexpression of SOD1 in transgenic rats attenuates nuclear translocation of endonuclease G and apoptosis after spinal cord injury.

Authors: Yu, F  Sugawara, T  Nishi, T  Liu, J  Chan, PH 
Citation: Yu F, etal., J Neurotrauma. 2006 May;23(5):595-603.
RGD ID: 8655990
Pubmed: PMID:16689664   (View Abstract at PubMed)
DOI: DOI:10.1089/neu.2006.23.595   (Journal Full-text)

Spinal motor neurons are selectively vulnerable after spinal cord injury (SCI). Recent studies suggest they undergo apoptosis after caspase activation through a mitochondria-dependent apoptosis pathway, and that oxidative stress after SCI is likely to play a role. However, other signaling pathways of apoptosis that involve mitochondria have not been thoroughly studied after SCI. Apoptosis-inducing factor (AIF) and endonuclease G (EndoG) are mitochondrial apoptogenic proteins that are capable of inducing neuronal apoptosis when translocated from mitochondria to nuclei through a caspase-independent pathway. In this study, we examined translocation of these proteins and apoptotic cell death of motor neurons. The role of oxidative stress was also studied using transgenic (Tg) rats that overexpress the intrinsic antioxidant copper/zinc-superoxide dismutase (SOD1). Western blots and an activity assay demonstrated that a greater amount of SOD1 and higher activity of SOD presented in mitochondria of Tg rats compared with wild-type (Wt) rats. Immunohistochemistry and Western blots showed translocation of EndoG and AIF from mitochondria to nuclei in motor neurons 1 day after SCI in both groups of rats. However, there was significantly less translocation of EndoG in the Tg rats compared with the Wt rats. Less apoptotic cell death was detected in the Tg rats than in the Wt rats 3 days after SCI. These results suggest that translocation of EndoG and AIF from mitochondria to nuclei may initiate a caspase-independent pathway of apoptosis. An increased level of SOD1 in mitochondria conceivably reduces oxidative stress, thereby attenuating EndoG translocation, and resulting in reduction of caspase-independent apoptosis.

RGD Manual Disease Annotations    Click to see Annotation Detail View
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
Spinal Cord Injuries  ISOEndog (Rattus norvegicus)8655990; 8655990 RGD 
Spinal Cord Injuries  IEP 8655990 RGD 
Spinal Cord Injuries treatmentIMP 8655990human gene in a rat modelRGD 
Spinal Cord Injuries treatmentISOSOD1 (Homo sapiens)8655990; 8655990human gene in a rat modelRGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Cellular Component
TermQualifierEvidenceWithReferenceNotesSourceOriginal Reference(s)
perikaryon  IDA 8655990 RGD 

Objects Annotated

Genes (Rattus norvegicus)
Endog  (endonuclease G)
Sod1  (superoxide dismutase 1)

Genes (Mus musculus)
Endog  (endonuclease G)
Sod1  (superoxide dismutase 1, soluble)

Genes (Homo sapiens)
ENDOG  (endonuclease G)
SOD1  (superoxide dismutase 1)


Additional Information