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Yu S.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Shu H.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Yang T.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Huang H.,General Hospital of the Peoples Liberation Army Chengdu Military Region | And 3 more authors.
Biochemical and Biophysical Research Communications | Year: 2016

Nogo-A and its receptor (NgR) were first described as myelin-associated inhibitors of neuronal regeneration in response to injury. In recent years, knowledge about the important role of the Nogo-A protein in several neuronal pathologies has grown considerably. Here, we employed a neonatal cortex freeze-lesion (NFL) model in neonatal rats and measured the expression of Nogo-A and NgR in the resulting cerebrocortical microdysgenesis 5-75 days after freezing injury. We observed marked upregulation of Nogo-A and NgR in protein levels. Furthermore, the migration of neural precursor cells (NPCs) derived from the subventricular zone (SVZ) toward the sits of injury was perturbed by treatment of NgR antagonist peptide NEP1-40. In vitro analysis showed that the knockdown of NgR by lentivirus-delivered siRNA promoted in axonal regeneration and SVZ-derived neural stem cell/progenitor cell (SVZ-NPCs) adhesion and migration, findings which were similar to the effects of NEP1-40. Taken together, our results indicate an important role for NgR in regulating the physiological processes of SVZ-NPCs. The observation of upregulated Nogo-A/NgR in lesion sites in the NFL model suggest that the effects of the perturbed Nogo-A are a key feature during the development and/or the progression of cortical malformation. © 2016 Elsevier Inc.


Shu H.-F.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Shu H.-F.,Chongqing Medical University | Kuang Y.-Q.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Liu S.-Y.,Chongqing Medical University | And 5 more authors.
Journal of Molecular Neuroscience | Year: 2014

Microgyria is associated with epilepsy and due to developmental disruption of neuronal migration. However, the role of endogenous subventricular zone-derived neural progenitors (SDNPs) in formation and hyperexcitability has not been fully elucidated. Here, we establish a neonatal cortex freeze-lesion (FL) model, which was considered as a model for focal microgyria, and simultaneously label SDNPs by CM-DiI. Morphological investigation showed that SDNPs migrated into FL and differentiated into neuronal and glia cell types, suggesting the involvement of endogenous SDNPs in the formation of FL-induced microgyria. Patch-clamp recordings in CM-DiI positive (CM-DiI+) pyramidal neurons within FL indicated an increase in frequency of spontaneous action potentials, while the resting membrane potential did not differ from the controls. We also found that spontaneous excitatory postsynaptic currents (EPSCs) increased in frequency but not in amplitude compared with controls. The evoked EPSCs showed a significant increase of 10-90 % in rise time and decay time in the CM-DiI+ neurons. Moreover, paired-pulse facilitation was dramatically larger in CM-DiI+ pyramidal neurons. Western blotting data showed that AMPA and NMDA receptors were increased to some extent in the FL cortex compared with controls, and the NMDA/AMPA ratio of eEPSCs at CM-DiI + pyramidal neurons was significantly increased. Taken together, our findings provide novel evidence for the contribution of endogenous SDNPs in the formation and epileptogenicity of FL-induced focal microgyria. © 2013 Springer Science+Business Media.


Gong G.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Hu L.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Liu Y.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Bai S.,General Hospital of the Peoples Liberation Army Chengdu Military Region | And 5 more authors.
International Journal of Molecular Medicine | Year: 2014

Cerebral ischemia/reperfusion (I/R) can induce neuronal death, particularly in the hippocampal formation (HF). Molecular genetic studies have suggested that the activities of the transcription factor, hypoxia-inducible factor-1α (HIF-1α), are closely linked to ischemia-induced neuronal death. However, the mechanisms through which HIF-1α functions remain poorly understood. In this study, primary cortical neurons were subjected to oxygen-glucose deprivation (OGD) to establish a cell model of OGD/reperfusion (RP). HIF-1α mRNA and protein expression was measured by qRT-PCR and western blot analysis. Cell proliferation was detected by MTT assay. Flow cytometric analysis was used to detect cell apoptosis and changes in mitochondrial mass. The expression of LC3-I and LC3-II was examined by western blot analysis. We found that HIF-1α increased cell proliferation and decreased cell apoptosis in our cell model of OGD/RP using cultured neonatal rat cortical neurons. The overexpression of HIF-1α significantly induced changes in mitochondrial mass and mitochondrial autophagy in cortical neurons. Moreover, the inhibition of HIF-1α markedly suppressed cell proliferation and mitochondrial autophagy. We also demonstrated that the HIF-1α-induced mitochondrial autophagy was accompanied by the inhibition of the mTOR pathway. This study provides direct in vitro evidence that HIF-1α overexpression triggers mitochondrial autophagy, thereby increasing neuronal survival. Our results highlight a novel target molecule toward which anti-ischemic neuroprotective effects can be applied.


Shu H.-F.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Yang T.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Yu S.-X.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Huang H.-D.,General Hospital of the Peoples Liberation Army Chengdu Military Region | And 3 more authors.
PLoS ONE | Year: 2014

Background: Although some trials assessed the effectiveness of aerobic exercise for Parkinson's disease (PD), the role of aerobic exercise in the management of PD remained controversial. Objective: The purpose of this systematic review is to evaluate the evidence about whether aerobic exercise is effective for PD. Methods: Seven electronic databases, up to December 2013, were searched to identify relevant studies. Two reviewers independently extracted data and assessed methodological quality based on PEDro scale. Standardised mean difference (SMD) and 95% confidence intervals (CI) of random-effects model were calculated. And heterogeneity was assessed based on the I2 statistic. Results: 18 randomized controlled trials (RCTs) with 901 patients were eligible. The aggregated results suggested that aerobic exercise should show superior effects in improving motor actions (SMD, 20.57; 95% CI 20.94 to 2 0.19; p = 0.003), balance (SMD, 2.02; 95% CI 0.45 to 3.59; p = 0.01), and gait (SMD, 0.33; 95% CI 0.17 to 0.49; p <0.0001) in patients with PD, but not in quality of life (SMD, 0.11; 95% CI 20.23 to 0.46; p = 0.52). And there was no valid evidence on follow-up effects of aerobic exercise for PD. Conclusion: Aerobic exercise showed immediate beneficial effects in improving motor action, balance, and gait in patients with PD. However, given no evidence on follow-up effects, large-scale RCTs with long follow-up are warrant to confirm the current findings. © 2014 Shu et al.


Huang H.-D.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Yang C.-M.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Shu H.-F.,General Hospital of the Peoples Liberation Army Chengdu Military Region | Kuang Y.-Q.,General Hospital of the Peoples Liberation Army Chengdu Military Region | And 7 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

Stroke, either ischemic or hemorrhagic, is the leading cause of death and morbidity worldwide. Identifying the risk factors is a prerequisite step for stroke prevention and treatment. It is believed that a major portion of the currently unidentified risk factors is of genetic origin. Consistent with this idea, numerous potential risk alleles for stroke have been reported, however, the genetic evidence so far is not conclusive. The major goal of this review is to update the current knowledge about the genetic predisposition to the common multifactorial stroke, and to provide a bird’s-eye view of this fast moving field. We selectively review and meta-analyze the related English literatures in public domain (PubMed) from 2000 onward, including the original reports and meta-analyses, to evaluate the genetic risk factors of common multifactorial stroke. The results indicated that we reviewed and meta-analyzed original reports and existing meta-analyses that studied the genetic predisposition to the common multifactorial stroke. Some original reports and meta-analyses were specific for ischemic stroke and others were for hemorrhagic stroke only. We also evaluated the major evolving issues in this field and discussed the future directions. In conclusion, strong evidences suggest that genetic risk factors contribute to common multifactorial stroke, and many genetic risk genes have been implicated in the literatures. However, not a single risk allele has been conclusively approved. © 2015, E-Century Publishing Corporation. All rights reserved.

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