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05 May 2013, Volume 8 Issue 13 Previous Issue    Next Issue

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Inhibition of inflammatory mediator release from microglia can treat ischemic/hypoxic brain injury Huaibo Wang, Weitao Guo, Hongliang Liu, Rong Zeng, Mingnan Lu, Ziqiu Chen, Qixian Xiao 2013, 8 (13):  1157-1168.  doi: 10.3969/j.issn.1673-5374.2013.13.001 Abstract ( 224 )   PDF (375KB) ( 1097 )   Save Interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inflammatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β. References | Related Articles | Metrics

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Does closure of acid-sensing ion channels reduce ischemia/reperfusion injury in the rat brain? Jie Wang, Yinghui Xu, Zhigang Lian, Jian Zhang, Tingzhun Zhu, Mengkao Li, Yi Wei, Bin Dong 2013, 8 (13):  1169-1179.  doi: 10.3969/j.issn.1673-5374.2013.13.002 Abstract ( 201 )   PDF (256KB) ( 848 )   Save null References | Related Articles | Metrics

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Rho kinase A new target for treatment of cerebral ischemia/reperfusion injury Qinghong Cui, Yongbo Zhang, Hui Chen, Jimei Li 2013, 8 (13):  1180-1189.  doi: 10.3969/j.issn.1673-5374.2013.13.003 Abstract ( 214 )   PDF (261KB) ( 1127 )   Save null References | Related Articles | Metrics

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Are human dental papilla-derived stem cell and human brain-derived neural stem cell transplantations suitable for treatment of Parkinson’s disease? Hyung Ho Yoon, Joongkee Min, Nari Shin, Yong Hwan Kim, Jin-Mo Kim, Yu-Shik Hwang, Jun-Kyo Francis Suh, Onyou Hwang, Sang Ryong Jeon 2013, 8 (13):  1190-1200.  doi: 10.3969/j.issn.1673-5374.2013.13.004 Abstract ( 199 )   PDF (662KB) ( 1019 )   Save Transplantation of neural stem cells has been reported as a possible approach for replacing impaired dopaminergic neurons. In this study, we tested the efficacy of early-stage human dental papilla-derived stem cells and human brain-derived neural stem cells in rat models of 6-hydroxydopamine-induced Parkinson’s disease. Rats received a unilateral injection of 6-hydroxydopamine into right medial forebrain bundle, followed 3 weeks later by injections of PBS, early-stage human dental papilla-derived stem cells, or human brain-derived neural stem cells into the ipsilateral striatum. All of the rats in the human dental papilla-derived stem cell group died from tumor formation at around 2 weeks following cell transplantation. Postmortem examinations revealed homogeneous malignant tumors in the striatum of the human dental papilla-derived stem cell group. Stepping tests revealed that human brain-derived neural stem cell transplantation did not improve motor dysfunction. In apomorphine-induced rotation tests, neither the human brain-derived neural stem cell group nor the control groups (PBS injection) demonstrated significant changes. Glucose metabolism in the lesioned side of striatum was reduced by human brain-derived neural stem cell transplantation. [18F]-FP-CIT PET scans in the striatum did not demonstrate a significant increase in the human brain-derived neural stem cell group. Tyrosine hydroxylase (dopaminergic neuronal marker) staining and G protein-activated inward rectifier potassium channel 2 (A9 dopaminergic neuronal marker) were positive in the lesioned side of striatum in the human brain-derived neural stem cell group. The use of early-stage human dental papilla-derived stem cells confirmed its tendency to form tumors. Human brain-derived neural stem cells could be partially differentiated into dopaminergic neurons, but they did not secrete dopamine. References | Related Articles | Metrics

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Are bone marrow regenerative cells ideal seed cells for the treatment of cerebral ischemia? Yi Li, Xuming Hua, Fang Hua, Wenwei Mao, Liang Wan, Shiting Li 2013, 8 (13):  1201-1209.  doi: 10.3969/j.issn.1673-5374.2013.13.005 Abstract ( 143 )   PDF (243KB) ( 832 )   Save Bone marrow cells for the treatment of ischemic brain injury may depend on the secretion of a large number of neurotrophic factors. Bone marrow regenerative cells are capable of increasing the secretion of neurotrophic factors. In this study, after tail vein injection of 5-fluorouracil for 7 days, bone marrow cells and bone marrow regenerative cells were isolated from the tibias and femurs of rats, and then administered intravenously via the tail vein after focal cerebral ischemia. Immunohistological staining and reverse transcription-PCR detection showed that transplanted bone marrow cells and bone marrow regenerative cells could migrate and survive in the ischemic regions, such as the cortical and striatal infarction zone. These cells promote vascular endothelial cell growth factor mRNA expression in the ischemic marginal zone surrounding the ischemic penumbra of the cortical and striatal infarction zone, and have great advantages in promoting the recovery of neurological function, reducing infarct size and promoting angiogenesis. Bone marrow regenerative cells exhibited stronger neuroprotective effects than bone marrow cells. Our experimental findings indicate that bone marrow regenerative cells are preferable over bone marrow cells for cell therapy for neural regeneration after cerebral ischemia. Their neuroprotective effect is largely due to their ability to induce the secretion of factors that promote vascular regeneration, such as vascular endothelial growth factor. References | Related Articles | Metrics

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Stem cell properties and neural differentiation of sheep amniotic epithelial cells Xuemin Zhu, Xiumei Wang, Guifang Cao, Fengjun Liu, Yinfeng Yang, Xiaonan Li, Yuling Zhang, Yan Mi, Junping Liu, Lingli Zhang 2013, 8 (13):  1210-1219.  doi: 10.3969/j.issn.1673-5374.2013.13.006 Abstract ( 199 )   PDF (341KB) ( 1249 )   Save This study was designed to verify the stem cell properties of sheep amniotic epithelial cells and their capacity for neural differentiation. Immunofluorescence microscopy and reverse transcription-PCR revealed that the sheep amniotic epithelial cells were positive for the embryonic stem cell marker proteins SSEA-1, SSEA-3, SSEA-4, TRA-1-60 and TRA-1-81, and the totipotency-associated genes Oct-4, Sox-2 and Rex-1, but negative for Nanog. Amniotic epithelial cells expressed β-III-tubulin, glial fibrillary acidic protein, nestin and microtubule-associated protein-2 at 28 days after induction with serum-free neurobasal-A medium containing B-27. Thus, sheep amniotic epithelial cells could differentiate into neurons expressing β-III-tubulin and microtubule-associated protein-2, and glial-like cells expressing glial fibrillary acidic protein, under specific conditions. References | Related Articles | Metrics

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Hyperbaric oxygen treatment promotes neural stem cell proliferation in the subventricular zone of neonatal rats with hypoxic-ischemic brain damage Zhichun Feng, Jing Liu, Rong Ju1, 2013, 8 (13):  1220-1227.  doi: 10.3969/j.issn.1673-5374.2013.13.007 Abstract ( 168 )   PDF (532KB) ( 1057 )   Save null References | Related Articles | Metrics

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Angiotensinogen gene polymorphism and ischemic stroke in East Asians Sheng Wang, Rong Zeng, Limin Lei, Jinsong Huang 2013, 8 (13):  1228-1235.  doi: 10.3969/j.issn.1673-5374.2013.13.008 Abstract ( 176 )   PDF (257KB) ( 1000 )   Save OBJECTIVE: To investigate the association between angiotensinogen gene M235T polymorphism and ischemic stroke in East Asians. DATA RETRIEVAL: A computer-based online search was conducted in PubMed, Google scholar, China National Knowledge lnfrastructure database between January 1990 and April 2012 for relevant studies. The key words were angiotensinogen or AGT, polymorphism or genetic and ischemic stroke or cerebral infarction. SELECTION CRITERIA: Case-controlled studies addressing the correlation between angiotensinogen gene M235T polymorphism and ischemic stroke in East Asians were included. The distribution of genotypes in the included studies was tested for Hardy-Weinberg equilibrium. Quality evaluation of the included studies was conducted by two physicians. Statistical analyses were carried out using Stata 12.0 software for meta-analysis. Heterogeneity tests, sensitivity analysis and publication bias were also conducted. MAIN OUTCOME MEASURES: The association between angiotensinogen gene M235T polymorphism and ischemic stroke risk in East Asians was assessed. RESULTS: Six relevant studies involving 891 patients with ischemic stroke and 727 controls were included in this meta-analysis. Results showed that there was a significant association between angiotensinogen gene M235T polymorphism and the risk of ischemic stroke in East Asians (T vs. M: odds ratio (OR) = 1.54, 95% confidence interval (CI) = 1.10–2.16; TT vs. MM: OR = 2.24, 95%CI = 1.37–3.66; TT vs. MT: OR = 1.76, 95%CI = 1.41–2.20; MM + MT vs. TT: OR = 0.57, 95%CI = 0.46–0.70). Sensitivity analysis confirmed that the study results were stable and reliable, with no publication bias. CONCLUSION: The angiotensinogen gene M235T polymorphism is associated with ischemic stroke in East Asians, and the TT genotype and T allele are risk factors for ischemic stroke. References | Related Articles | Metrics

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Communicating with the non-dominant hemisphere Implications for neurological rehabilitation Fabricio Ferreira de Oliveira, Sheilla de Medeiros Correia Marin, Paulo Henrique Ferreira Bertolucci 2013, 8 (13):  1236-1246.  doi: 10.3969/j.issn.1673-5374.2013.13.009 Abstract ( 233 )   PDF (154KB) ( 985 )   Save Aphasic syndromes usually result from injuries to the dominant hemisphere of the brain. Despite the fact that localization of language functions shows little interindividual variability, several brain areas are simultaneously activated when language tasks are undertaken. Mechanisms of language recovery after brain injury to the dominant hemisphere seem to be relatively stereotyped, including activations of perilesional areas in the acute phase and of homologues of language areas in the non-dominant hemisphere in the subacute phase, later returning to dominant hemisphere activation in the chronic phase. Plasticity mechanisms reopen the critical period of language development, more specifically in what leads to disinhibition of the non-dominant hemisphere when brain lesions affect the dominant hemisphere. The non-dominant hemisphere plays an important role during recovery from aphasia, but currently available rehabilitation therapies have shown limited results for efficient language improvement. Large-scale randomized controlled trials that evaluate well-defined interventions in patients with aphasia are needed for stimulation of neuroplasticity mechanisms that enhance the role of the non-dominant hemisphere for language recovery. Ineffective treatment approaches should be replaced by more promising ones and the latter should be evaluated for proper application. The data generated by such studies could substantiate evidence-based rehabilitation strategies for patients with aphasia. References | Related Articles | Metrics