RGD Reference Report - Over-expression of PUMA correlates with the apoptosis of spinal cord cells in rat neuropathic intermittent claudication model. - Rat Genome Database

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Over-expression of PUMA correlates with the apoptosis of spinal cord cells in rat neuropathic intermittent claudication model.

Authors: Ma, B  Shi, J  Jia, L  Yuan, W  Wu, J  Fu, Z  Wang, Y  Liu, N  Guan, Z 
Citation: Ma B, etal., PLoS One. 2013 May 2;8(5):e56580. doi: 10.1371/journal.pone.0056580. Print 2013.
RGD ID: 9586024
Pubmed: (View Article at PubMed) PMID:23658678
DOI: Full-text: DOI:10.1371/journal.pone.0056580

BACKGROUND: Neuropathic intermittent claudication (NIC) is a typical clinical symptom of lumbar spinal stenosis and the apoptosis of neurons caused by cauda equina compression (CEC) has been proposed as an important reason. Whereas, the factors and the mechanism involved in the process of apoptosis induced by CEC remain unclear. METHODOLOGY AND RESULTS: In our modified rat model of NIC, a trapezoid-shaped silicon rubber was inserted into the epidural space under the L5 and L6 vertebral plate. Obvious apoptosis was observed in spinal cord cells after compression by TUNEL assay. Simultaneously, qRT-PCR and immunohistochemistry showed that the expression levels of PUMA (p53 up-regulated modulator of apoptosis) and p53 were upregulated significantly in spinal cord under compression, while the expression of p53 inhibitor MDM2 and SirT2 decreased in the same region. Furthermore, CEC also resulted in the upregulation of Bcl-2 pro-apoptotic genes expression and caspase-3 activation. With the protection of Methylprednisolone, the upregulation of PUMA and p53 expression as well as the decrease of MDM2 and SirT2 in spinal cord were partially rescued in western bolt analysis. CONCLUSIONS: These results suggest that over-expression of PUMA correlates with CEC caused apoptosis of spinal cord cells, which is characterized by the increase of p53, Bax and Bad expression. PUMA upregulation might be crucial to induce apoptosis of spinal cord cells through p53-dependent pathway in CEC.



Disease Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Bad  (BCL2-associated agonist of cell death)
Bak1  (BCL2-antagonist/killer 1)
Bax  (BCL2 associated X, apoptosis regulator)
Bbc3  (Bcl-2 binding component 3)
Casp3  (caspase 3)
Mdm2  (MDM2 proto-oncogene)
Sirt2  (sirtuin 2)

Genes (Mus musculus)
Bad  (BCL2-associated agonist of cell death)
Bak1  (BCL2-antagonist/killer 1)
Bax  (BCL2-associated X protein)
Bbc3  (BCL2 binding component 3)
Casp3  (caspase 3)
Mdm2  (transformed mouse 3T3 cell double minute 2)
Sirt2  (sirtuin 2)

Genes (Homo sapiens)
BAD  (BCL2 associated agonist of cell death)
BAK1  (BCL2 antagonist/killer 1)
BAX  (BCL2 associated X, apoptosis regulator)
BBC3  (BCL2 binding component 3)
CASP3  (caspase 3)
MDM2  (MDM2 proto-oncogene)
SIRT2  (sirtuin 2)


Additional Information