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  • Title: Effects of magnetically labeled exogenous endothelial progenitor cells on cerebral blood perfusion and microvasculature alterations after traumatic brain injury in rat model.
    Author: Chen X, Yin J, Wu X, Li R, Fang J, Chen R, Zhang B, Zhang W.
    Journal: Acta Radiol; 2013 Apr 01; 54(3):313-23. PubMed ID: 23528570.
    Abstract:
    BACKGROUND: Increasing evidence suggests that endothelial progenitor cells (EPCs), a subgroup of bone marrow hematopoietic stromal cells, play a critical role in neovascularization and tissue repair. PURPOSE: To explore the effect of exogenous EPCs on the cerebral blood perfusion and microvessels in the injured region in rat model with traumatic brain injury (TBI). MATERIAL AND METHODS: EPCs were collected from the spleens of healthy Sprague-Dawley rats. Fifty-four Sprague-Dawley rats were randomly divided into six groups. The controlled cortical impact TBI was performed. Spleen-derived exogenous EPCs labeled with super-paramagnetic iron oxide (SPIO) (SPIO-EPCs) were transplanted into the blood by tail vein of rats at 6 and 12 h after TBI, respectively. Magnetic resonance imaging (MRI) and computed tomography perfusion imaging were performed at various time points. Microvascular density was determined by immunohistochemistry. RESULTS: In SPIO-EPCs group, patchlike hypointensities were detected in the injured region at 24 h after transplantation, and the range of hypointensities tended to expand gradually over time on MRI, which was confirmed by Prussian blue staining. Computed tomography perfusion imaging parameters were gradually developed from hyperperfusion to normal, while, microvascular density was gradually increased during 72 to 168 h after injury. The values of these indices in SPIO-EPCs group were significantly lower than those in SPIO-alone group at the same time point, but no significant differences were found in different time groups. CONCLUSION: The intravenously transplanted EPCs diminish the brain injury through restoring cerebral blood perfusion and increasing the cerebral microvasculature in the injured region in rat model with TBI.
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