Reduction in antioxidant enzyme expression and sustained inflammation enhance tissue damage in the subacute phase of spinal cord contusive injury
Open Access
- 7 February 2011
- journal article
- Published by Springer Science and Business Media LLC in Journal of Biomedical Science
- Vol. 18 (1), 13
- https://doi.org/10.1186/1423-0127-18-13
Abstract
Traumatic spinal cord injury (SCI) forms a disadvantageous microenvironment for tissue repair at the lesion site. To consider an appropriate time window for giving a promising therapeutic treatment for subacute and chronic SCI, global changes of proteins in the injured center at the longer survival time points after SCI remains to be elucidated. Through two-dimensional electrophoresis (2DE)-based proteome analysis and western blotting, we examined the differential expression of the soluble proteins isolated from the lesion center (LC) at day 1 (acute) and day 14 (subacute) after a severe contusive injury to the thoracic spinal cord at segment 10. In situ apoptotic analysis was used to examine cell apoptosis in injured spinal cord after adenoviral gene transfer of antioxidant enzymes. In addition, administration of chondroitinase ABC (chABC) was performed to analyze hindlimb locomotor recovery in rats with SCI using Basso, Beattie and Bresnahan (BBB) locomotor rating scale. Our results showed a decline in catalase (CAT) and Mn-superoxide dismutase (MnSOD) found at day 14 after SCI. Accordingly, gene transfer of SOD was introduced in the injured spinal cord and found to attenuate cell apoptosis. Galectin-3, β-actin, actin regulatory protein (CAPG), and F-actin-capping protein subunit β (CAPZB) at day 14 were increased when compared to that detected at day 1 after SCI or in sham-operated control. Indeed, the accumulation of β-actin+ immune cells was observed in the LC at day 14 post SCI, while most of reactive astrocytes were surrounding the lesion center. In addition, chondroitin sulfate proteoglycans (CSPG)-related proteins with 40-kDa was detected in the LC at day 3-14 post SCI. Delayed treatment with chondroitinase ABC (chABC) at day 3 post SCI improved the hindlimb locomotion in SCI rats. Our findings demonstrate that the differential expression in proteins related to signal transduction, oxidoreduction and stress contribute to extensive inflammation, causing time-dependent spread of tissue damage after severe SCI. The interventions by supplement of anti-oxidant enzymes right after SCI or delayed administration with chABC can facilitate spinal neural cell survival and tissue repair.Keywords
This publication has 43 references indexed in Scilit:
- T-LAK Cell-originated Protein Kinase (TOPK) Phosphorylation of Prx1 at Ser-32 Prevents UVB-induced Apoptosis in RPMI7951 Melanoma Cells through the Regulation of Prx1 Peroxidase ActivityPublished by Elsevier BV ,2010
- Peroxiredoxin 6 Fails to Limit Phospholipid Peroxidation in Lung from Cftr-Knockout Mice Subjected to Oxidative ChallengePLOS ONE, 2009
- Involvement of Acidic Fibroblast Growth Factor in Spinal Cord Injury Repair Processes Revealed by a Proteomics ApproachMolecular & Cellular Proteomics, 2008
- Fate of endogenous stem/progenitor cells following spinal cord injuryJournal of Comparative Neurology, 2006
- Detection of sequence-specific tyrosine nitration of manganese SOD and SERCA in cardiovascular disease and agingAmerican Journal of Physiology-Heart and Circulatory Physiology, 2006
- Proteomic analysis of injured spinal cord tissue proteins using 2-DE and MALDI-TOF MSProteomics, 2006
- Inflammation, degeneration and regeneration in the injured spinal cord: insights from DNA microarraysTrends in Neurosciences, 2003
- Clearing a path for nerve growthNature, 2002
- Diffusion barriers evoked in the rat cortex by reactive astrogliosisGlia, 1999
- MASCIS Evaluation of Open Field Locomotor Scores: Effects of Experience and Teamwork on ReliabilityJournal of Neurotrauma, 1996