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Beijing, China

Fa Z.,Zhujiang Hospital | Fa Z.,Neurosurgery Institute | Zhang P.,Zhujiang Hospital | Zhang P.,Neurosurgery Institute | And 15 more authors.
Neurological Research | Year: 2011

Objective: Functional neuroimaging techniques act as the navigator to assess changes in brain activity induced by repetitive transcranial magnetic stimulation (rTMS) in rTMS studies. The aim of this study was to investigate the feasibility of using manganese-enhanced magnetic resonance imaging (MEMRI) to measure the brain activity in rTMS studies. Methods: Eighteen Wistar rats were randomized into three groups (n56) including a high rTMS group, a low rTMS group and a sham stimulation group (controls). They were given rTMS of 10 Hz, 1 Hz or sham stimulation for 5 hours separately. MEMRI was used to assess the changes of brain activity. Results: Compared with the controls, image intensity was enhanced differently in various brain regions on T1-weighted images after rTMS with different frequencies, higher intensity and wider enhancement occurred in the high frequency rTMS group as compared with that in the low frequency rTMS group. Conclusion: MEMRI can be used to reveal the changes of brain activity in live rats following rTMS. Significance: The current experiment might provide a new functional neuroimaging technique for the study of rTMS. © W. S. Maney & Son Ltd 2011. Source


Dong Y.,Harbin Medical University | Jia L.,Harbin Medical University | Wang X.,Harbin Medical University | Tan X.,Harbin Medical University | And 6 more authors.
International Journal of Oncology | Year: 2011

Clinical studies using the tyrosine kinase inhibitor, imatinib mesylate (Gleevec®), in glioblastoma, have shown no major inhibition of tumor growth or extension of survival for patients, unlike those in chronic myeloid leukemia (CML) and gastrointestinal stromal tumors. The molecular mechanisms of action of imatinib in glioblastoma cells are still not well understood. In this study, we investigated the effects of imatinib on the platelet derived growth factor receptor (PDGFR) downstream signaling pathways as well as on other cellular functions in human glioblastoma cells. NIH3T3 fibroblast and K562 CML cells were used for comparison. Western blot analysis demonstrated that imatinib was more effective in inhibiting the activated rather than the quiescent forms of the target proteins. Furthermore, the imatinib treatment induced the sustained activation of extracellular signal-regulated kinase (ERK 1/2) signaling as well as components of other downstream signaling pathways, such as PI3K/Akt, STAT3 and p38MAPK. Prior stimulation of the malignant cells with exogenous PDGF-BB partially abrogated this activation. Further analysis indicated that the activation of ERK induced by the imatinib treatment was related to the S-phase re-entry of the cell cycle in one of the three glioma cells. Imatinib significantly inhibited cell migration but not cell growth. The combination treatment of imatinib with a MEK or PI3K inhibitor resulted in significant growth inhibition but did not inhibit cell migration beyond the inhibition achieved with the imatinib treatment alone. The treatment of glioma cells with small interfering RNA inhibiting PDGFRB, however, evoked enhanced Akt signaling. These results indicate that the imatinib treatment of malignant glioma does not result in significant inhibitory effects and should be used with caution. Source


Dong Y.,Harbin Medical University | Dong Y.,Immunity and Infection Key Laboratory of Heilongjiang Province | Han Q.,Harbin Medical University | Han Q.,Immunity and Infection Key Laboratory of Heilongjiang Province | And 14 more authors.
Molecular and Cellular Biochemistry | Year: 2012

Glioblastoma multiforme (GBM) was shown to harbor therapy-resistant cancer stem cells that were major causes of recurrence. PDGFR (platelet-derived growth factor receptor) and c-Kit (stem cell factor receptor) signaling play important roles in initiation and maintenance of malignant glioma. This study demonstrated that long-term culture with imatinib mesylate, the tyrosine kinase inhibitor against PDGFR and c-Kit resulted in reduced cancer stem cell ability in glioblastoma cells through cell differentiation. Derived from RG glioblastoma cells co-cultured with imatinib for 3 months, RG-IM cells showed distinct properties of cell cycle distribution and morphology in addition to significantly decreased ability to form aggregates and colonies in vitro and tumorigenicity in vivo. Increased expression of GFAP (astrocyte marker) and class III β-tubulin isotype (Tuj1, neuron marker) were detected with morphology like neurons or astrocytes in RG-IM cells. Furthermore, decreased expression of stem cell markers, i.e., CD133, Oct-3/4, nestin, and Bmi1, and increased terminal neural cell markers, GFAP, Tuj1, etc., were identified in RG-IM at the mRNA level. All these markers were changed in RG cells when PDGFRB and c-Kit expression were double knocked down by siRNA. Cell differentiation agent, all-trans retinoic acid (ATRA) caused similar effect as that with imatinib in RG cells, while adding PDGF-B and SCF in RG-IM resulted in cell dedifferentiation to some extent. Moreover, differentiation in RG cells treated by imatinib or ATRA was mainly driven by MAPK signaling pathways. In summary, continuous inhibition on PDGFR and c-Kit signaling disturbed glioma stem cells biology in subsets of GBM cells and may have potentials in clinical applications. © 2012 Springer Science+Business Media, LLC. Source


Cheng G.,Neurosurgery Institute | Cheng G.,Chinese PLA General Hospital | Zhang H.,Neurosurgery Institute | Zhang H.,Chinese PLA General Hospital | And 4 more authors.
Tumor Biology | Year: 2015

The molecular regulation of the growth of glioblastoma (GBM) is not completely understood. Here, we show that the Cyr61 levels were significantly higher in GBM than in the adjacent non-tumor tissues. Overexpression of Cyr61 enhanced the viability of GBM cells, while inhibition of Cyr61 decreased the viability of GBM cells, in vitro and in vivo. Further analyses revealed that Cyr61 seemed to activate PI3K/Akt/mTor signaling pathway to increase cell growth in GBM cells. Taken together, our findings suggest a potential role of Cyr61 in GBM growth and highlight Cyr61 as a novel target for GBM therapy. © 2014, International Society of Oncology and BioMarkers (ISOBM). Source

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