Tianjin Key Laboratory of Injuries

Tianjin, China

Tianjin Key Laboratory of Injuries

Tianjin, China
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Wang Z.,Tianjin Medical University | Wang Z.,Tianjin Neurologic Institute | Wang Z.,Key Laboratory of Post Trauma Neuro Repair and Regeneration in Central Nervous System | Wang Z.,Tianjin Key Laboratory of Injuries | And 7 more authors.
Journal of Molecular Neuroscience | Year: 2013

Bone marrow stromal cells (MSCs) were used as cell therapy for various diseases in recent years. Some reports showed that transplanted MSCs promote functional recovery in animal models of brain trauma. But other studies indicate that tissue replacement by this method may not be the main source of therapeutic benefit. Neurotrophic factors such as brain-derived neurotrophic factor (BDNF) therapeutic potential may contribute to the recovery of function after trauma. Our previous study showed that BDNF-MSCs could promote the survival of neurons in neuronal injured models in vitro. The present study was undertaken to explore the therapeutic effects of MSCs transfected with BDNF in vivo. After intraventricular injection of MSCs-BDNF, BDNF levels were increased significantly in cerebrospinal fluid by ELISA. Further studies showed that treatment of traumatic brain injury with MSCs-BDNF could attenuate neuronal injury as measurement of biological behavior assessment. These studies demonstrate that by increasing the brain concentration of BDNF, intraventricularly transplanted MSCs-BDNF might play an important role in the treatment of traumatic brain injury and might be an optional therapeutic strategy. © 2012 Springer Science+Business Media New York.


Wang L.,Peking Union Medical College | Shi C.,Tianjin Medical University | Shi C.,Tianjin Key Laboratory of Injuries | Shi C.,Key Laboratory of Post trauma Neuro repair and Regeneration in Central Nervous System | And 2 more authors.
Neuroscience Letters | Year: 2014

Recent work suggests that women have a higher liability to major depressive disorder (MDD) than men, but the mechanism for the gender difference remains unknown. Given a genetic component involved in MDD, genome-wide association studies (GWAS) have been performed to search for susceptibility loci for the diseases and several genes of interest have been reported, including the EH-domain containing 3 (EHD3) gene that encodes a protein participating in endosome protein trafficking. However, the polymorphism association of the EHD3 gene with MDD failed to be replicated in a Chinese Han population. In the present study, we stratified 517 MDD patients and 455 control subjects by gender and symptoms and found 3 SNPs present in the EHD3 gene, of which rs619002 and rs644926 were exclusively associated with female MDD (p=0.0045 and p=0.0074, respectively) and rs649729 (p=0.0029) was closely related to anxious mood of female patients, suggesting a gender-specific role of EHD3 in MDD. These positive findings help explain, at least from one aspect, the poor replication of GWAS results. Further functional analysis is needed to clarify how variants in EHD3 may play a female-specific role in the pathogenesis of MDD. © 2014 Elsevier Ireland Ltd.


Yang X.,China National Academy of Nanotechnology and Engineering | Yang X.,Tianjin Medical University | Yang X.,Tianjin Neurological Institute | Yang X.,Key Laboratory Of Post Trauma Neuro Repair And Regeneration In Control Nerv Systems | And 11 more authors.
Chemical Research in Toxicology | Year: 2012

Recent studies have proved that zinc oxide nanoparticles (nZnO) can cause acute lung epithelial inflammation and respiratory toxicity; however, the mechanism of such acute negative effect on lung epithelia is still unclear. In this study, early responses of living human alveolar epithelial A549 cells after exposure to nZnO were investigated by noncontact hopping probe ion conductance microscopy (HPICM) that was combined with the patch-clamp technique. Continuous repetitive high-resolution HPICM scannings observed that 100 μg/mL nZnO treatment caused acute damage to A549 cell membrane within 1.5 h. Such membrane (Figure presented) damage was reflected in a significantly elevated lactate dehydrogenase (LDH) level in cell culture medium after 3 h of nZnO exposure. The combined HPICM and patch-clamp technique can easily perform whole-cell patch-clamp recordings, which demonstated that nZnO treatment even could inhibit the activities of ion channels in A549 cells within 15 min. The HPICM technique is shown to be capable of detecting the acute toxicity of nZnO on living cells in real time and helping to elucidate the mechanism of its action. © 2011 American Chemical Society.


Yang X.,China National Academy of Nanotechnology and Engineering | Liu X.,China National Academy of Nanotechnology and Engineering | Zhang X.,China National Academy of Nanotechnology and Engineering | Lu H.,China National Academy of Nanotechnology and Engineering | And 4 more authors.
Ultramicroscopy | Year: 2011

PC12 cells derived from rat pheochromocytoma can differentiate into sympathetic-neuron-like cells in response to nerve growth factor (NGF). These cells have been proved to be a useful cell model to study neuronal differentiation. NGF induces rapid changes in membrane morphology, neurite outgrowth, and electrical excitability. However, the relationship between the 3D morphological changes of NGF-differentiated PC12 cells and their electrophysiological functions remains poorly understood.In this study, we combined a recently developed Hopping Probe Ion Conductance Microscopy (HPICM) with patch-clamp technique to investigate the high-resolution morphological changes and functional ion-channel development during the NGF-induced neuronal differentiation of PC12 cells. NGF enlarged TTX-sensitive sodium currents of PC12 cells, which associated with cell volume, membrane surface area, surface roughness of the membrane, and neurite outgrowth. These results demonstrate that the combination of HPICM and patch-clamp technique can provide detailed information of membrane microstructures and ion-channel functions during the differentiation of PC12 cells, and has the potential to become a powerful tool for neuronal research. © 2011 Elsevier B.V.


Ning X.,Tianjin Medical University | Shi Z.,Tianjin Medical University | Shi Z.,Tianjin Neurological Institute | Shi Z.,Key Laboratory of Post trauma Neuro repair and Regeneration in Central Nervous System | And 17 more authors.
Cancer Letters | Year: 2015

Aberrant expression of the microRNA-200 (miR-200) family has been linked to the occurrence and development of various types of malignant tumors, including hepatocellular carcinoma (HCC), colon cancer and breast cancer. However, little is known about the precise mechanism by which miR-200 expression is downregulated. The intricate relationship between DNA methylation and histone modifications has become a subject of increasing interest. The expression of miR-200 family members is modified by similar or complementary epigenetic mechanisms in MGC-803 and BGC-823 gastric cancer cells and U87 MG glioma cells. Chromatin immunoprecipitation assays revealed that DNA methyltransferase 1 (DNMT1) bound to miR-200b/a/429 promoter regions, indicating an interaction between DNMT1 and the miR-200b/a/429 promoter. Furthermore, Co-Immunoprecipitation (Co-IP) detection showed that DNMT1, together with the PcG protein Enhancer of Zeste homolog 2 (EZH2), a histone methyltransferase, contributed to the transcriptional repression of microRNA-200 family members. Knockdown of EZH2 not only impacted H3K27 trimethylation but also reduced DNMT1 presence on the miR-200b/a/429 promoter. EZH2 appeared to be essential for DNMT1 recruitment to the promoter region. Silencing EZH2 and DNMT1 using drugs or RNA interference dramatically reduced the levels of miR-200b/a/429 expression. Collectively, these results indicated that EZH2 and DNMT1-mediated epigenetic silencing contributed to the progression of gastric cancer and glioblastoma, and therefore represents a novel therapeutic target for malignant tumors. © 2015 Elsevier Ireland Ltd.


Gong D.,Royal Melbourne Hospital | Gong D.,Tianjin Medical University | Gong D.,Tianjin Neurological Institute | Gong D.,Key Laboratory of Post trauma Neuro repair and Regeneration in Central Nervous System | And 4 more authors.
Journal of Stroke and Cerebrovascular Diseases | Year: 2014

We describe a case of successful management of a growing basilar artery dissecting aneurysm by the Pipeline flow diversion embolization device (PED). A 48-year-old woman presented with severe headache, neck pain, and altered consciousness. Computed tomography showed subarachnoid hemorrhage located in basal cisterns, with a pontine infarct shown on magnetic resonance imaging. Digital subtraction angiography showed dissecting aneurysm of the trunk of the basilar artery, with growth over time on repeated imaging. Repeated imaging demonstrated growth in size of the aneurysm. The aneurysm was treated with PED with complete obliteration of the basilar artery aneurysm. Subsequent follow-up demonstrated good clinical recovery. © 2014 by National Stroke Association.


Liu Z.,Fifth Central Hospital of Tianjin | Jiang Z.,Fifth Central Hospital of Tianjin | Huang J.,Duke University | Huang S.,Duke University | And 7 more authors.
International Journal of Oncology | Year: 2014

Epidermal growth factor receptor (EGFR) signaling regulates glioblastoma cell proliferation, survival, migration and invasion and plays a key role in tumor progression. We show that microRNA-7 (miR-7) is a common regulator of the phosphoinositide-3-kinase (PI3K)/ATK and Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathways, both of which are launched by EGFR through its two direct targets, the transcription factors PI3K and Raf-1, respectively. Enforced expression of miR-7 markedly decreased expression of PI3K, phosphorylated Akt, Raf-1, phosphorylated MEK 1/2, and cyclin D1, as well as slightly reduced expression of EGFR. Forced expression of PI3K or Raf-1 transcripts lacking the 3′-untranslated region (3′-UTR) partially reversed the effects of miR-7 on cell growth inhibition and cell cycle arrest in glioma cells. Additionally, transient expression of miR-7 in glioblastoma cells strongly inhibited in vivo glioblastoma xenograft growth. We conclude that miR-7 is a potential tumor suppressor in glioblastoma that acts by targeting multiple oncogenes related to the downstream pathway of EGFR and may serve as a novel therapeutic target for malignant gliomas.


Liu Z.,Fifth Central Hospital of Tianjin | Jiang Z.,Fifth Central Hospital of Tianjin | Huang J.,Duke University | Huang S.,Duke University | And 7 more authors.
International Journal of Oncology | Year: 2014

Intrinsic resistance of glioma cells to radiation and chemotherapy is currently hypothesized to be partially attributed to the existence of cancer stem cells. Emerging studies suggest that mesenchymal stem cells may serve as a potential carrier for delivery of therapeutic genes to disseminated glioma cells. However, the tropism character of mesenchymal stem cells for cancer stem cell-like glioma cells has rarely been described. In this study, we obtained homologous bone marrow-derived (BM-) and adipose tissue-derived (AT-) mesenchymal stem cells (MSCs), fibroblast, and cancer stem cell-like glioma cells (CSGCs) from tumor-bearing mice, and compared the tropism character of BM- and AT-MSCs for CSGCs with various form of existence. To characterize the cell proliferation and differentiation, the spheroids of CSGCs were cultured on the surface of the substrate with different stiffness, combined with or withdrew basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) in medium. Our results showed that the CSGCs during the process of cell proliferation, but not in resting and differentiated status, display strong tropism characteristics on both BM- and AT-MSCs, as well as the expression of their cell chemokine factors which mediate cell migration. If the conclusion is further confirmed, it may expose a fatal flaw of MSCs as tumor-targeted delivery of therapeutic agents in the treatment of the CSGCs, even other cancer stem cells, because there always exist a part of cancer stem cells that are in resting status. Overall, our findings provide novel insight into the complex issue of the MSCs as drug delivery in the treatment of brain tumors, especially in tumor stem cells.


Liu L.,Tianjin Medical University | Liu L.,Key Laboratory of Post Trauma Neuro Repair and Regeneration in Central Nervous System | Liu L.,Tianjin Key Laboratory of Injuries | Wei H.,Tianjin Medical University | And 12 more authors.
Critical Care Medicine | Year: 2011

Objective: Endothelial progenitor cells play an active role in vascular repair and revascularization of tissue damaged by traumatic, inflammatory, and ischemic injures. We correlate the changes in circulating endothelial progenitor cells with the severity of traumatic brain injury. The study is designed to investigate the endothelial progenitor cell mobilization after injury and a potential use of circulating endothelial progenitor cells as a prognostic marker for evaluating trauma severity and clinical outcomes. Design: A prospective cohort study conducted in two neurosurgical intensive care units of Tianjin Medical University General Hospital and Tianjin Huanhu Hospital (Tianjin, China). Patients: Patients with traumatic brain injury and age- and gender-matched healthy controls. Interventions: None. Measurements and Main Results: Changes in the levels of circulating endothelial progenitor cells were monitored for up to 21 days in 84 patients with traumatic brain injury. Results were correlated with the clinical assessment of injury severity as determined by the Glasgow Coma Scale. The level of circulating endothelial progenitor cells was found to be suppressed 24-48 hrs after injury but rapidly increased, reaching the highest at days 5-7 post-trauma. Circulating endothelial progenitor cells in patients with improved Glasgow Coma Scale scores were significantly higher than those with deteriorated conditions and remained persistently low in patients who died of trauma. Conclusions: The results suggest that the level of circulating endothelial progenitor cells correlates with the clinical severity and outcome of traumatic brain injury and may offer potential as a prognostic marker for traumatic brain injury. A long-term follow-up of these patients is ongoing. Copyright © 2011 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.


Zhang K.,Tianjin Medical University | Zhang K.,Tianjin Neurological Institute | Zhang K.,Key Laboratory of Post trauma Neuro repair and Regeneration in Central Nervous System | Zhang K.,Tianjin Key Laboratory of Injuries | And 16 more authors.
Journal of Neuroimmune Pharmacology | Year: 2012

Extensive data have shown that Wnt/beta-catenin signaling is associated with various disease pathologies, including an important role in tumorigenesis. Here, we review the regulation of Wnt/beta-catenin signaling in glioma, with particular focus on the expression signatures of the main components in Wnt/beta-catenin signaling, the role of key factors in Wnt/beta-catenin signaling, and crosstalk with other signaling pathways. Finally, we discuss the involvement of microRNAs in Wnt/beta-catenin signaling in glioma. This review reveals new insights into the role of Wnt/beta-catenin signaling in gliomagenesis, and highlights new therapeutic approaches for glioma, based on the modulation of the Wnt/beta-catenin pathway. © 2012 Springer Science+Business Media, LLC.

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