Vascular endothelial growth factor (VEGF) stimulation and bone marrow mesenchymal stem cell (BMSC) transplantation have been implicated in the treatment of acute cerebral infarction for their pivotal roles in behavioral recovery, neuroprotection, neurogenesis, and angiogenesis. However, the effects of BMSC transplants are likely limited because of low transplant survival after acute cerebral infarction, and delivery of VEGF alone also has limited effects on recovery because the protein is cleared quickly. This study attempted to explore whether VEGF could be transferred into BMSC via an adenovirus and whether transplanting VEGF-transfected BMSC into the rat brain provides sufficient neuroprotection after transient middle cerebral artery occlusion. The adenovirus carried VEGF into BMSC (Ad-VEGF-BMSC), and purified adenovirus was transferred into BMSC (Ad-BMSC). Western blots were used to detect the expression of VEGF protein after transfection. Rats exposed to 90-min middle cerebral artery occlusion (MCAO) were treated with Ad-VEGF-BMSC, Ad-BMSC, BMSC and Dulbecco's Modified Eagle's Medium (DMEM) after ischemia reperfusion for 24h. The Sham group only received surgery. After transplantation of Ad-VEGF-BMSC into the perifocal area of the ischemic rat brain, we found increased expression and secretion of VEGF and BDNF as well as a higher level of MAP2, increased microvascular density, improved behavioral function and enhanced BMSC survival. Our results indicated that transplantation of Ad-VEGF-BMSC improved ischemic neurological deficiency after MCAO in rats. This finding provides a potential valuable therapeutic intervention for cerebral ischemic diseases.

01 Apr 2013·Journal of NeuroimmunologyQ3 · MEDICINE

The immunomodulatory effect of bone marrow stromal cells (BMSCs) on interleukin (IL)-23/IL-17-mediated ischemic stroke in mice

Q3 · MEDICINE

Article

Author: Yanyan Sun ; Yi Zheng ; Jian Luo ; Guozhong Li ; Yanhong Yin ; Hongping Chen ; Di Zhong ; Hulun Li ; Shuainan Ma

Ischemic cerebral infarction is a leading cause of death and disability, but the key inflammatory cytokines were not fully understood and no successful therapy has been established. We have used the methods of reverse transcriptase-polymerase chain reaction (RT-PCR), enzyme-linked immunosorbent assay (ELISA), western blot, and immunohistochemical staining to detect the dynamic changes of IL-23/IL-17 axis in brain infarction and BMSC treatment on the sixth day. BMSC transplantation could reduce the infarct size (P<0.05) and improve functional deficits (P<0.001) in brain infarction. The level of IL-23/IL-17 axis expression is higher (P<0.05) in pMCAO-operated group than that in sham operated group. BMSC treatment could reduce IL-23 expression (P<0.05) and attenuate IL-17 expression (P<0.01) both in serum and around infarct lesion. So we have drawn the conclusion that IL-23/IL-17 axis induces inflammation in the pathophysiological process of cerebral infarction. BMSC treatment plays therapeutic role by immunomodulating the expression of IL-23/IL-17 axis. These findings may help to understand the cytokines in cerebral infarction and open up a possible new way of immunological treatment.

01 Jan 2013·Journal of Nuclear MedicineQ1 · MEDICINE

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

Q1 · MEDICINE

Article

Author: Houkin, Kiyohiro ; Miyamoto, Michiyuki ; Shichinohe, Hideo ; Magota, Keiichi ; Tamaki, Nagara ; Kuroda, Satoshi ; Zhao, Songji ; Kuge, Yuji

This study aimed to assess whether (18)F-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.METHODSThe 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 (18)F-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.RESULTSBMSC 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.CONCLUSIONThe 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. (18)F-FDG PET may be a valuable modality to scientifically prove the beneficial effects of BMSC transplantation on the host brain in clinical situations.

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Indication	Highest Phase	Country/Location	Organization	Date
Osteoarthritis	Preclinical	CN	Ever Supreme Bio Technology Co., Ltd.	05 Sep 2024
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