The Expression and Function of the Tumor Necrosis Factor Receptor I (TNFRI), TNFRII, and X-Linked Inhibitor of Apoptosis Genes after Spinal Cord Injury in Rats.
10.4184/jkss.2004.11.1.14
- Author:
Jun Young YANG
1
;
June Kyu LEE
;
Kyung Tae KIM
;
Hyun Ho LEE
;
Byung Nam BYUN
;
Sung Hwan AHN
Author Information
1. Department of Orthopaedic Surgery, School of Medicine, Chungnam National University, Daejon, Korea. jyyang@cnuh.co.kr
- Publication Type:Original Article
- Keywords:
Spinal cord injury;
TNFRI;
TNFRII;
XIAP
- MeSH:
Animals;
Apoptosis*;
Gene Expression;
Halothane;
In Situ Hybridization;
Necrosis;
Neurons;
Oligodendroglia;
Rats*;
Rats, Sprague-Dawley;
Receptors, Tumor Necrosis Factor*;
Spinal Cord Diseases;
Spinal Cord Injuries*;
Spinal Cord*;
Spine;
Tumor Necrosis Factor-alpha*;
Up-Regulation
- From:Journal of Korean Society of Spine Surgery
2004;11(1):14-23
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
STUDY DESIGN AND OBJECTIVE: Tumor necrosis factor-alpha(TNF-alpha), a key inflammatory mediator, has been demonstrated in spinal cord injury (SCI). However, the expression of TNF receptors following SCI remains to be identified. To elucidate the expressions of TNF receptor I (TNFRI), TNFRII, XIAP, and their function in SCI, in situ hybridization and RT-PCR were performed in a SCI model. MATERIAL AND METHODS: Sprague-Dawley rats were anesthetized with halothane and laminectomized at the level of the eleventh and twelfth thoracic vertebra. Using a modified New York University Impactor, SCI was induced by dropping a 10 gm weight from a height of 20 mm. The rod of the impactor had a constant circular surface, 3 mm in diameter. After induction of the injury, rats were placed in a temperature and humidity-controlled chamber overnight. RESULTS: The TNFRI gene was not detected in the control rats, but the TNFRII gene was expressed in the neurons in the control rats. The TNFRI gene expression was maximally increased in the spinal cord 1 day after the SCI; however, that of the TNFRII gene occurred 3 days after the SCI. In the white matter, both the TNFRI and TNFRII genes were increased in the oligodendrocytes 3 days after the SCI. The XIAP gene was increased in neurons of the gray matter 1 and 3 days after the SCI, but was not detected in the white matter after the SCI. CONCLUSION: Up-regulation of the expression of TNFRII occurs later than that of TNFRI in the spinal cord after a SCI. TNFR may be related to neuronal survival considering its similar expression pattern to that of XIAP. The results from these studies may lead to alternative therapeutic targets of TNF receptors in spinal cord injury, providing the basis for developing agonist and antagonist systems for TNF receptor subtypes and also for encouraging better strategies for the treatment of spinal cord disorders related to trauma.
