Calpain activity and translational expression increased in spinal cord injury

Calpain, a calcium-activated neutral proteinase, has been implicated in myelin and cytoskeletal protein degradation following spinal cord injury. In the present study, we examined the activity and transcriptional expression of calpain in spinal cord injury lesions via Western blotting analysis and R...

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Bibliographic Details
Published in:Brain research 1999-01, Vol.816 (2), p.375-380
Main Authors: Ray, Swapan K., Shields, Donald C., Saido, Takaomi C., Matzelle, Denise C., Wilford, Gloria G., Hogan, Edward L., Banik, Naren L.
Format: Article
Language:English
Subjects:
Animals
Biochemistry and metabolism
Biological and medical sciences
Blotting, Western
Calcium
Calpain
Calpain - metabolism
Calpastatin
Carrier Proteins - metabolism
Central nervous system
Female
Fluorescent Antibody Technique
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation, Enzymologic
Hydrolysis
Microfilament Proteins - metabolism
Nerve Tissue Proteins - metabolism
Neutral proteinase
Protein Biosynthesis
Rats
Rats, Sprague-Dawley
Reverse Transcriptase Polymerase Chain Reaction
Spinal Cord Injuries - metabolism
Spinal cord injury
Vertebrates: nervous system and sense organs
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Summary:Calpain, a calcium-activated neutral proteinase, has been implicated in myelin and cytoskeletal protein degradation following spinal cord injury. In the present study, we examined the activity and transcriptional expression of calpain in spinal cord injury lesions via Western blotting analysis and RT-PCR, respectively. No increases in transcriptional expression of calpain or calpastatin, the endogenous inhibitor, were observed in the lesion at 1, 4, 24, and 72 h following injury. However, calpain activity (as measured by calpain-specific degradation of the endogenous substrate fodrin) was marginally increased at 4 h and significantly increased by 129.8% at 48 h compared to sham controls after injury. Calpain translational expression was localized in injured spinal cords using double immunofluorescent labeling which revealed increased calpain expression in astrocytes compared to sham controls. These results suggest that calpain produced by astrocytes located in or near spinal cord injury lesions may participate in myelin/axon degeneration following injury.
ISSN:0006-8993
1872-6240
DOI:10.1016/S0006-8993(98)01128-7