INTRODUCTION: This study was to evaluate the in vivo distribution of intravenously transplanted bone marrow-derived mesenchymal stem cells (BMSCs) in an acute brain trauma model by (111)In-tropolone labeling. METHODS: Rat BMSCs were labeled with 37 MBq (111)In-tropolone. Their labeling efficiency and in vitro retention rate were measured. The viability and proliferation of labeled BMSCs were evaluated for 14 days after labeling. The biodistribution of (111)In-labeled BMSCs in trauma models was compared with those of sham-operated rats and normal rats on gamma camera images. The migration of (111)In-BMSCs to the traumatic brain was evaluated using confocal microscope. RESULTS: The labeling efficiency of (111)In-BMSCs was 66+/-5%, and their retention rate was 85.3% at 1 h after labeling. There was no difference in the number of viable cells between (111)In-BMSCs and controls at 48 h after labeling. However, the proliferation of (111)In-BMSCs was inhibited after the third day of labeling, and it did not reach confluency. On gamma camera images, most of the (111)In-BMSCs uptake was observed in the liver and spleen at the second day of injection. The brain uptake of (111)In-BMSCs was detected prominently in trauma models (1.4%) than in sham-operated (0.5%) or normal rats (0.3%). Radiolabeled BMSCs were observed at the traumatic brain on the confocal microscope as they have a homing capacity, although its proliferation capacity was suppressed. CONCLUSION: Although growth inhibition by (111)In-labeling need to be evaluated further prior to use in humans, (111)In-labeled BMSCs are useful for the tracking of intravenously transplanted mesenchymal stem cells in brain disease models. Copyright 2010 Elsevier Inc. All rights reserved.
INTRODUCTION: This study was to evaluate the in vivo distribution of intravenously transplanted bone marrow-derived mesenchymal stem cells (BMSCs) in an acute brain trauma model by (111)In-tropolone labeling. METHODS:Rat BMSCs were labeled with 37 MBq (111)In-tropolone. Their labeling efficiency and in vitro retention rate were measured. The viability and proliferation of labeled BMSCs were evaluated for 14 days after labeling. The biodistribution of (111)In-labeled BMSCs in trauma models was compared with those of sham-operated rats and normal rats on gamma camera images. The migration of (111)In-BMSCs to the traumatic brain was evaluated using confocal microscope. RESULTS: The labeling efficiency of (111)In-BMSCs was 66+/-5%, and their retention rate was 85.3% at 1 h after labeling. There was no difference in the number of viable cells between (111)In-BMSCs and controls at 48 h after labeling. However, the proliferation of (111)In-BMSCs was inhibited after the third day of labeling, and it did not reach confluency. On gamma camera images, most of the (111)In-BMSCs uptake was observed in the liver and spleen at the second day of injection. The brain uptake of (111)In-BMSCs was detected prominently in trauma models (1.4%) than in sham-operated (0.5%) or normal rats (0.3%). Radiolabeled BMSCs were observed at the traumatic brain on the confocal microscope as they have a homing capacity, although its proliferation capacity was suppressed. CONCLUSION: Although growth inhibition by (111)In-labeling need to be evaluated further prior to use in humans, (111)In-labeled BMSCs are useful for the tracking of intravenously transplanted mesenchymal stem cells in brain disease models. Copyright 2010 Elsevier Inc. All rights reserved.
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