The role of thrombospondin-1 and transforming growth factor-beta after spinal cord injury in the rat

Spinal cord injury (SCI) continues to result in high morbidity and mortality throughout the world. An effective neuroprotective agent is still not available to counteract secondary damage caused by traumatic injury. Thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) have a role in angiogenesis, scar deposition, inflammation and may affect astrocyte phenotype and mobility. We investigated the role of TSP-1 and TGF-beta in a model of spinal cord injury in rats. Forty female Sprague-Dawley rats were randomly divided into two equal groups: the experimental group was subject to SCI using an impactor and the sham-operated group was not subject to SCI. These animals were sacrificed at 12 h and 24 h after SCI for immunochemistry and Western blot analysis of the injured spinal segment for the expression of the TSP-1 and TGF-beta proteins. We found that TSP-1 and TGF-beta expression increased immediately after SCI in the injured segment. After 12 h, TSP-1 concentrations increased more rapidly and dramatically than TGF-beta in the injured segment of the spinal cord. Elevations in TSP-1 and TGF-beta concentrations persisted for 24 h after injury. These results show that elevated expression of TSP-1 and TGF-beta can be detected in the injured segment of the spinal cord 12 and 24 h after injury. Thus, TSP-1 and TGF-beta may have a role in SCI.