Bone Marrow Stromal Cell Transplantation Enhances Recovery of Local Glucose Metabolism After Cerebral Infarction in Rats: A Serial 18F-FDG PET Study

被引:32
|
作者
Miyamoto, Michiyuki
Kuroda, Satoshi [1 ]
Zhao, Songji [2 ]
Magota, Keiichi [3 ]
Shichinohe, Hideo
Houkin, Kiyohiro
Kuge, Yuji [4 ]
Tamaki, Nagara [3 ]
机构
[1] Hokkaido Univ, Grad Sch Med, Dept Neurosurg, Kita Ku, Sapporo, Hokkaido 0608638, Japan
[2] Hokkaido Univ, Grad Sch Med, Dept Tracer Kinet & Bioanal, Sapporo, Hokkaido 0608638, Japan
[3] Hokkaido Univ, Grad Sch Med, Dept Nucl Med, Sapporo, Hokkaido 0608638, Japan
[4] Hokkaido Univ, Cent Inst Isotope Sci, Sapporo, Hokkaido 0608638, Japan
关键词
cerebral infarct; bone marrow stromal cell; transplantation; F-18-FDG; PET; INJURED SPINAL-CORD; IN-VIVO; FUNCTIONAL RECOVERY; ACID RECEPTOR; ADULT-RAT; BRAIN; ISCHEMIA; STROKE; MICE; DIFFERENTIATE;
D O I
10.2967/jnumed.112.109017
中图分类号
R8 [特种医学]; R445 [影像诊断学];
学科分类号
1002 ; 100207 ; 1009 ;
摘要
This study aimed to assess whether F-18-FDG PET could serially monitor the beneficial effects of bone marrow stromal cells (BMSC) on cerebral glucose metabolism when transplanted into the infarct brain of rats. Methods: The BMSC from green fluorescent protein transgenic rats or vehicle was stereotactically transplanted into the ipsilateral striatum at 7 d after permanent middle cerebral artery occlusion of rats. Local glucose metabolism was semiquantitatively measured at 6 and 35 d after ischemia using F-18-FDG PET. Motor function was serially evaluated throughout the experiments. At 35 d after ischemia, immunohistochemistry was performed to evaluate the phenotype of BMSC and their effects on the expression of brain-type glucose transporters. Results: BMSC transplantation not only enhanced functional recovery but also promoted the recovery of glucose utilization in the periinfarct area when stereotactically transplanted at 1 wk after ischemia. The engrafted cells were widely distributed, and most expressed a neuron-specific protein, NeuN. BMSC transplantation also prevented the pathologic upregulation of glucose transporters in the periinfarct neocortex. Conclusion: The present findings strongly suggest that the BMSC may enhance functional recovery by promoting the recovery of local glucose metabolism in the periinfarct area when directly transplanted into the infarct brain at clinically relevant timing. The BMSC also inhibit the pathologic upregulation of brain-isoform glucose transporters type 1 and 3. F-18-FDG PET may be a valuable modality to scientifically prove the beneficial effects of BMSC transplantation on the host brain in clinical situations.
引用
收藏
页码:145 / 150
页数:6
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