BACKGROUND: Spinal cord injury (SCI) is a common and often irreversible lesion that can incapacitate patients. Precursor cells in the spinal cord proliferate in response to trauma, and this proliferation can be enhanced by exogenous stimuli such as specific growth factors. In the present study, we examined electron microscopic detection of the proliferation, distribution, and phenotypic fate of these precursor cells in the injured adult rat spinal cord. METHODS: Adult female Sprague-Dawley rats weighing 250 to 300 g were divided into 3 groups. The first group consisted of spinal cord-injured animals with application of a 2.4-g clip extradurally around the spinal cord at the T1 level. A 26-g clip was applied in the second group. The third group included normal uninjured animals. Rats were sacrificed at 3 days, 3 weeks, and 6 weeks after injury. A segment of the spinal cord, 0.4 cm in length, encompassing the injury site was removed and was prepared for electron microscopy. RESULTS: Three days after mild injury (2.4-g clip), ependymal cells had begun to proliferate and had migrated from the central canal. They had a tendency to surround perivascular spaces close to the axons. The central canal rostral to the lesion site was widely dilated at 6 weeks postoperative in the moderately injured groups (26-g clip). The layer of ependymal cells lining the dilated canal showed reduction in cell height. Traumatic syringomyelic cavities were observed in all of the animals. There was an active proliferative response of the ependymal cells to injury. Large clusters of displaced ependymal cells associated with the dilated central canal were observed. Rests of ependymal cells were observed remote from the central canal with a tendency to form rosettes and accessory lumina 6 weeks after trauma. Fascicles of 3 to 8 fibers enclosed within an ependymal cell were a common finding among the ependymal clusters. There were also debris and some ependymal cells in the lumen. CONCLUSION: Trauma induces active proliferation of precursor cells in the ependymal region. These cells may replace neural tissue lost to SCI and may assist in axonal regeneration.
BACKGROUND:Spinal cord injury (SCI) is a common and often irreversible lesion that can incapacitate patients. Precursor cells in the spinal cord proliferate in response to trauma, and this proliferation can be enhanced by exogenous stimuli such as specific growth factors. In the present study, we examined electron microscopic detection of the proliferation, distribution, and phenotypic fate of these precursor cells in the injured adult rat spinal cord. METHODS: Adult female Sprague-Dawley rats weighing 250 to 300 g were divided into 3 groups. The first group consisted of spinal cord-injured animals with application of a 2.4-g clip extradurally around the spinal cord at the T1 level. A 26-g clip was applied in the second group. The third group included normal uninjured animals. Rats were sacrificed at 3 days, 3 weeks, and 6 weeks after injury. A segment of the spinal cord, 0.4 cm in length, encompassing the injury site was removed and was prepared for electron microscopy. RESULTS: Three days after mild injury (2.4-g clip), ependymal cells had begun to proliferate and had migrated from the central canal. They had a tendency to surround perivascular spaces close to the axons. The central canal rostral to the lesion site was widely dilated at 6 weeks postoperative in the moderately injured groups (26-g clip). The layer of ependymal cells lining the dilated canal showed reduction in cell height. Traumatic syringomyelic cavities were observed in all of the animals. There was an active proliferative response of the ependymal cells to injury. Large clusters of displaced ependymal cells associated with the dilated central canal were observed. Rests of ependymal cells were observed remote from the central canal with a tendency to form rosettes and accessory lumina 6 weeks after trauma. Fascicles of 3 to 8 fibers enclosed within an ependymal cell were a common finding among the ependymal clusters. There were also debris and some ependymal cells in the lumen. CONCLUSION:Trauma induces active proliferation of precursor cells in the ependymal region. These cells may replace neural tissue lost to SCI and may assist in axonal regeneration.
Authors: Vicki M Tysseling; Divakar S Mithal; Vibhu Sahni; Derin Birch; Hosung Jung; Abdelhak Belmadani; Richard J Miller; John A Kessler Journal: J Neuroinflammation Date: 2011-02-16 Impact factor: 8.322
Authors: Jacek M Kwiecien; Wojciech Dabrowski; Beata Dąbrowska-Bouta; Grzegorz Sulkowski; Wendy Oakden; Christian J Kwiecien-Delaney; Jordan R Yaron; Liqiang Zhang; Lauren Schutz; Barbara Marzec-Kotarska; Greg J Stanisz; John P Karis; Lidia Struzynska; Alexandra R Lucas Journal: PLoS One Date: 2020-03-19 Impact factor: 3.240