Tao Jiang

Beijing Neurosurgical Institute, Peping, Beijing, China

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Publications (344)1386.03 Total impact

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    ABSTRACT: Arachidonyl-2-chloroethylamide (ACEA), a highly selective agonist of cannabinoid receptor 1 (CB1R), has been reported to protect neurons in ischemic injury. We sought to investigate whether mitochondrial biogenesis was involved in the therapeutic effect of ACEA in cerebral ischemia. Focal cerebral ischemic injury was induced in adult male Sprague Dawley rats. Intraperitoneal injection of 1 mg/kg ACEA improved neurological behavior, reduced infarct volume, and inhibited apoptosis. The volume and numbers of mitochondria were significantly increased after ACEA administration. Expression of mitochondrial transcription factor A (Tfam), nuclear transcription factor-1 (Nrf-1), and cytochrome C oxidase subunit IV (COX IV) were also significantly up-regulated in animals administered ACEA. One thousand nanomoles of ACEA inhibited mitochondrial dysfunction in primary rat cortical neurons exposed to oxygen-glucose deprivation (OGD). Furthermore, ACEA administration increased phosphorylation of glycogen synthase kinase-3β (GSK-3β) after reperfusion. Phosphorylation of GSK-3β induced mitochondrial biogenesis and preserved mitochondrial function whereas inhibition of phosphatidylinositol 3-kinase (PI3K) dampened phosphorylation of GSK-3β and reversed induction of mitochondrial biogenesis and function following ACEA administration. In conclusion, ACEA could induce mitochondrial biogenesis and improve mitochondrial function at the beginning of cerebral ischemia, thus alleviating cerebral ischemia injury. Phosphorylation of GSK-3β might be involved in the regulation of mitochondrial biogenesis induced by ACEA.
    No preview · Article · Jan 2016 · Molecular Neurobiology
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    ABSTRACT: Objective Pituitary adenomas are benign neoplasms that display invasive behavior—a characteristic traditionally associated with malignancy—through an ill-defined mechanism. The role of angiogenesis-related molecules in this pathological condition remains perplexing. Our purpose is to assess the impact of endocan (endothelial cell specific molecule-1, ESM-1), CD34 and CD105 on pituitary adenoma invasion. Methods In this study, immunohistochemical analyses for endocan, CD34 and CD105 were performed on paraffin-embedded samples of 66 pituitary adenomas, five normal pituitaries, and five primary hepatic carcinomas. Knosp tumor grades based on magnetic resonance imaging coronal scanning were used to assess the invasiveness of each sample. The associations between endocan expression, CD34/CD105-positive microvessel densities (MVDs), and Knosp tumor invasion grades were evaluated. Results These results showed that endocan protein expression in tumor cells (TCs) was higher than that in endothelial cells (ECs) and strongly correlated with Knosp grades (P < 0.001, Spearman’s r = 0.616). Moreover, while endocan-positive TCs localized around the blood vessels in adenomas with higher Knosp grades, no significant association was found between CD34/CD105-MVDs and Knosp grades (CD34: P = 0.256, r = 0.142; CD105: P = 0.183, r = 0.166). Normal pituitary seemed to exhibit lower endocan expression and contained more CD34/CD105-MVDs than pituitary adenomas. Conclusion Endocan expresses in both TCs and ECs of pituitary adenoma. Endocan overexpression in TCs more accurately reflects invasiveness compared to that of CD34/CD105-MVDs and that angiogenesis may not be the primary driver of endocan-medicated pituitary adenoma invasion.
    No preview · Article · Jan 2016 · Pituitary
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    ABSTRACT: Introduction Contrast enhancement observable on magnetic resonance (MR) images reflects the destructive features of malignant gliomas. This study aimed to investigate the relationship between radiologic patterns of tumor enhancement, extent of resection, and prognosis in patients with anaplastic gliomas (AGs). Methods Clinical data from 268 patients with histologically confirmed AGs were retrospectively analyzed. Contrast enhancement patterns were classified based on preoperative T1-contrast MR images. Univariate and multivariate analyses were performed to evaluate the prognostic value of MR enhancement patterns on progression-free survival (PFS) and overall survival (OS). Results The pattern of tumor contrast enhancement was associated with the extent of surgical resection in AGs. A gross total resection was more likely to be achieved for AGs with focal enhancement than those with diffuse (p = 0.001) or ring-like (p = 0.024) enhancement. Additionally, patients with focal-enhanced AGs had a significantly longer PFS and OS than those with diffuse (log-rank, p = 0.025 and p = 0.031, respectively) or ring-like (log-rank, p = 0.008 and p = 0.011, respectively) enhanced AGs. Furthermore, multivariate analysis identified the pattern of tumor enhancement as a significant predictor of PFS (p = 0.016, hazard ratio [HR] = 1.485) and OS (p = 0.030, HR = 1.446). Conclusion Our results suggested that the contrast enhancement pattern on preoperative MR images was associated with the extent of resection and predictive of survival outcomes in AG patients.
    No preview · Article · Jan 2016 · Neuroradiology

  • No preview · Article · Jan 2016 · The Journal of infection
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    ABSTRACT: RNA-RNAand protein-RNAinteractions are essential for post-transcriptionalregulationin normal development and may be deregulated in cancerinitiation and progression. The RNA-binding proteinPCBP2, an oncogenic protein in human malignant gliomas, is an essential regulator of mRNA and miRNA biogenesis, stability and activity.Here, we identified Rho GDP dissociation inhibitor α (ARHGDIA) as a target mRNA that binds to PCBP2, and we uncovered the role of ARHGDIA as a putative metastasis suppressor through analyses of in vitro and in vivo models of EMT and metastasis. Furthermore, we demonstrated that ARHGDIA is a potential target of miR-151-5p and miR-16 in gliomas. The interaction between PCBP2 and the 3'UTR of the ARHGDIA mRNA may induce a local change in RNA structure that favors subsequent binding of miR-151-5p and miR-16, thus leading to the suppression of ARHGDIA expression. PCBP2 may facilitate miR-151-5p and miR-16 promotion of glioma cell migration and invasion through mitigating the function of ARHGDIA.
    Preview · Article · Jan 2016 · Oncotarget
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    ABSTRACT: Glioblastoma (GBM) is one of the most lethal brain tumors with a short survival time. EGFR amplification and mutation is the most significant genetic signature in GBM. About half of the GBMs with EGFR amplification express a constitutively autophosphorylated variant of EGFR, known as EGFRvIII. Our in vitro data demonstrated further enhanced EGFRvIII activity and tumor cell invasion in the tumor microenvironment of hypoxia plus extracellular matrix (ECM) vitronectin, in which EGFRvIII and integrin β3 tended to form complexes. The treatment with ITGB3 siRNA or the integrin antagonist cilengetide preferentially interrupted the EGFRvIII/integrin β3 complex, effectively reduced tumor cell invasion and activation of downstream signaling effectors. Cilengitide is recently failed in Phase III CENTRIC trial in unselected patients with GBM. However, we found that cilengitide demonstrated efficacious tumor regression via inhibition of tumor growth and angiogenesis in EGFRvIII orthotopic xenografts. Bioinformatics analysis emphasized key roles of integrin β3, hypoxia and vitronectin and their strong correlations with EGFRvIII expression in malignant glioma patient samples in vivo. In conclusion, we demonstrate that EGFRvIII/integrin β3 complexes promote GBM progression and metastasis in the environment of hypoxia and vitronectin-enrichment, and cilengitide may serve as a promising therapeutics for EGFRvIII-positive GBMs.
    Full-text · Article · Dec 2015 · Oncotarget
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    ABSTRACT: Conventional therapeutic monoclonal antibodies (mAbs) are invalid for intracellular viruses but by using in situ biomineralization treatment, they can be successfully delivered into cells to inhibit intracellular viral replication. This achievement significantly expands the applications of mAbs and provides a new intracellular strategy to control viral infections.
    No preview · Article · Dec 2015 · Chemical Communications
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    ABSTRACT: Purpose: Epilepsy is one of the most common manifestations in gliomas and has a severe effect on the life expectancy and quality of life of patients. The aim of our study was to assess the potential connections between clinicopathological factors and postoperative seizure. Method: We retrospectively investigated a group of 147 Chinese high-grade glioma (HGG) patients with preoperative seizure to examine the correlation between postoperative seizure and clinicopathological factors and prognosis. Univariate analyses and multivariate logistic regression analyses were performed to identify factors associated with postoperative seizures. Survival function curves were calculated using the Kaplan-Meier method. Results: 53 patients (36%) were completely seizure-free (Engel class I), and 94 (64%) experienced a postoperative seizure (Engel classes II, III, and IV). A Chi-squared analysis showed that anaplastic oligodendroglioma/anaplastic oligoastrocytoma (AO/AOA) (P=0.05), epidermal growth factor receptor (EGFR) expression (P=0.0004), O(6)-methylguanine DNA methyltransferase (MGMT) expression (P=0.011), and phosphatase and tensin homolog (PTEN) expression (P=0.045) were all significantly different. A logistic regression analysis showed that MGMT expression (P=0.05), EGFR expression (P=0.001), and AO/AOA (P=0.038) are independent factors of postoperative seizure. Patients with lower MGMT and EGFR expression and AO/AOA showed more frequent instances of postoperative seizure. Postoperative seizure showed no statistical significance on overall survival (OS) and progression-free survival (PFS). Conclusion: Our study identified clinicopathological factors related to postoperative seizure in HGGs and found two predictive biomarkers of postoperative seizure: MGMT and EGFR. These findings provided insight treatment strategies aimed at prolonging survival and improving quality of life.
    No preview · Article · Dec 2015 · Seizure
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    ABSTRACT: Glioma is the most common malignant primary brain tumor among adults, among which glioblastoma (GBM) exhibits the highest malignancy. Despite current standard chemoradiation, glioma is still invariably fatal. A further insight into the molecular background of glioma is required to improve patient outcomes. Previous studies evaluated molecular genetic differences through comparing different grades of glioma. Here, we integrated DNA methylation, RNA sequencing and protein expression data sets of WHO grade II to IV gliomas, to screen for dysregulated genes in subtypes during malignant progression of glioma. We propose a list of universal genes (UG) as novel glioma biomarkers: 977 up-regulated genes and 114 down-regulated genes, who involved in cell cycle, Wnt receptor signaling pathway and fatty acid metabolic process. Poorer survival was associated significantly with the high expression of 977 up-regulated genes and low expression of 114 down-regulated in UG (P <0.001). To our knowledge, this was the first study that focused on subtypes to detect dysregulated genes that could contribute to malignant progression. Furthermore, the differentially expressed genes profile may lead to the identification of new therapeutic targets for glioma patients.
    Full-text · Article · Dec 2015 · Journal of Experimental & Clinical Cancer Research
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    ABSTRACT: Gliomas, the most common primary brain tumors, are characterized by isocitrate dehydrogenase 1 mutation (IDH1-M). High mutation frequency of IDH1 indicates it's promoting role in tumorgenesis. However, the observation that patients with IDH1-M have better survival comparing with patients with IDH1 wild-type (IDH1-W) suggests that this alteration has other significant beneficial features for patients. Currently, temozolomide (TMZ) is a standard of care for patients which play a major role in DNA methylation that is similar with the role of IDH1-M in genome-wide methylation. In this study, we collected 323 gliomas samples with genome-wide methylation microarray, 502 samples with genome-wide mRNA expression microarray and 295 samples with RNA-seq. By significance analysis of microarray (SAM), we identified 18 genes which are hypermethylation and low expression in samples with IDH1-M comparing with IDH1-W (FDR<0.01). Furthermore, 18 candidate genes were downregulated in TMZ-treated samples. Finally, we obtained two candidate genes, F3 and RBP1. Survival analysis showed that hypermethylation or low expression of the two genes indicated a favorable prognosis, which was consistent with IDH1-M and administration of TMZ in glioma patients. F3 and RBP1 were further validated by qPCR on an independent validation cohort containing 145 samples. Our data suggest that these candidate genes were suppressed by TMZ or IDH1-M induced hypermethylation, resulting in the favorable prognosis of patients with gliomas.
    No preview · Article · Nov 2015 · American Journal of Cancer Research
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    ABSTRACT: Aldehyde dehydrogenases (ALDH) is a family of enzymes including 19 members. For now, ALDH activity had been wildly used as a marker of cancer stem cells (CSCs). But biological functions of relevant isoforms and their clinical applications are still controversial. Here, we investigate the clinical significance and potential function of ALDH1A3 in gliomas. By whole-genome transcriptome microarray and mRNA sequencing analysis, we compared the expression of ALDH1A3 in high- and low- grade gliomas as well as different molecular subtypes. Microarray analysis was performed to identify the correlated genes of ALDH1A3. We further used Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis to explore the biological function of ALDH1A3. Finally, by mRNA knockdown we revealed the relationship between ALDH1A3 and the ability of tumor invasion. ALDH1A3 overexpression was significantly associated with high grade as well as the higher mortality of gliomas in survival analysis. ALDH1A3 was characteristically highly expressed in Mesenchymal (Mes) subtype gliomas. Moreover, we found that ALDH1A3 was most relevant to extracellular matrix organization and cell adhesion biological process, and the ability of tumor invasion was suppressed after ALDH1A3 knockdown in vitro. In conclusion, ALDH1A3 can serve as a novel marker of Mes phenotype in gliomas with potential clinical prognostic value. The expression of ALDH1A3 is associated with tumor cell invasion.
    Preview · Article · Nov 2015 · PLoS ONE
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    ABSTRACT: Oligodendrogliomas (ODs) are the second most common malignant brain tumor and exhibit characteristic co-deletion of chromosomal arms 1p and 19q (co-deletion 1p/19q), which is associated with down-regulation of tumor suppressors. However, co-deletion 1p/19q indicates a favorable prognosis that cannot be explained by the down-regulation of tumor suppressors. In the present study, we determined that co-deletion 1p/19q was associated with reduced Ki-67 protein level based on analysis of 354 ODs. To identify genes associated with reduced Ki-67 and a favorable prognosis of codeletion 1p/19q, we analyzed 96 ODs with RNA-sequencing and 136 ODs and 4 normal brain tissue samples with RNA microarrays. We thus identified seven genes within chromosomal arms 1p/19q with significantly reduced expression in samples with co-deletion of 1p/19q compared to samples with intact 1p/19q. A significant positive correlation was observed between these candidate genes and Ki-67 expression based on analysis of mRNA expression in 305 gliomas and 5 normal brain tissue samples. Survival analysis confirmed the prognostic value of these candidate genes. This finding suggests that these genes within chromosomal arms 1p/19q are associated with low Ki-67 and a favorable prognosis in ODs with co-deletion 1p/19q and provides novel therapeutic targets. © 2015 Wiley Periodicals, Inc.
    No preview · Article · Nov 2015 · Genes Chromosomes and Cancer
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    ABSTRACT: Background: The relative contribution of isocitrate dehydrogenase mutations (mIDH) and O6-methylguanine-DNA methyltransferase promoter methylation (methMGMT) as biomarkers in glioblastoma remain poorly understood. Methods: We investigated the association between methMGMT and mIDH with progression free survival and overall survival in a prospectively collected molecular registry of 274 glioblastoma patients. Results: For glioblastoma patients who underwent Temozolomide and Radiation Therapy, OS and PFS was most favorable for those with tumors harboring both mIDH and methMGMT (median OS: 35.8 mo, median PFS: 27.5 mo); patients afflicted glioblastomas with either mIDH or methMGMT exhibited intermediate OS and PFS (mOS: 36 and 17.1 mo; mPFS: 12.2 mo and 9.9 mo, respectively); poorest OS and PFS was observed in wild type IDH1 (wtIDH1) glioblastomas that were MGMT promoter unmethylated (mOS: 15 mo, mPFS: 9.7 mo). For patients with wtIDH glioblastomas, TMZ+RT was associated with improved OS and PFS relative to patients treated with RT (OS: 15.4 mo v 9.6 mo, p < 0.001; PFS: 9.9 mo v 6.5 mo, p < 0.001). While TMZ+RT and RT treated mIDH patients exhibited improved overall survival relative to those with wtIDH, there were no differences between the TMZ+RT or RT group. These results suggest that mIDH1 conferred resistance to TMZ. Supporting this hypothesis, exogenous expression of mIDH1 in independent astrocytoma/glioblastoma lines resulted in a 3-10 fold increase in TMZ resistance after long-term passage. Conclusion: Our study demonstrates IDH mutation and MGMT promoter methylation status independently associate with favorable outcome in TMZ+RT treated glioblastoma patients. However, these biomarkers differentially impact clinical TMZ response.
    Preview · Article · Oct 2015 · Oncotarget
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    ABSTRACT: The clinical prognosis of patients with glioma is determined by tumor grades, but tumors of different subtypes with equal malignancy grade usually have different prognosis that is largely determined by genetic abnormalities. Oligodendrogliomas (ODs) are the second most common type of gliomas. In this study, integrative analyses found that distribution of TCGA transcriptomic subtypes was associated with grade progression in ODs. To identify critical gene(s) associated with tumor grades and TCGA subtypes, we analyzed 34 normal brain tissue (NBT), 146 WHO grade II and 130 grade III ODs by microarray and RNA sequencing, and identified a co-expression network of six genes (AURKA, NDC80, CENPK, KIAA0101, TIMELESS and MELK) that was associated with tumor grades and TCGA subtypes as well as Ki-67 expression. Validation of the six genes was performed by qPCR in additional 28 ODs. Importantly, these genes also were validated in four high-grade recurrent gliomas and the initial lower-grade gliomas resected from the same patients. Finally, the RNA data on two genes with the highest discrimination potential (AURKA and NDC80) and Ki-67 were validated on an independent cohort (5 NBTs and 86 ODs) by immunohistochemistry. Knockdown of AURKA and NDC80 by siRNAs suppressed Ki-67 expression and proliferation of gliomas cells. Survival analysis showed that high expression of the six genes corporately indicated a poor survival outcome. Correlation and protein interaction analysis provided further evidence for this co-expression network. These data suggest that the co-expression of the six mitosis-regulating genes was associated with malignant progression and prognosis in ODs.
    Preview · Article · Oct 2015 · Oncotarget
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    ABSTRACT: Resistance to temozolomide poses a major clinical challenge in glioblastoma multiforme treatment, and the mechanisms underlying the development of temozolomide resistance remain poorly understood. Enhanced DNA repair and mutagenesis can allow tumour cells to survive, contributing to resistance and tumour recurrence. Here, using recurrent temozolomide-refractory glioblastoma specimens, temozolomide-resistant cells, and resistant-xenograft models, we report that loss of miR-29c via c-Myc drives the acquisition of temozolomide resistance through enhancement of REV3L-mediated DNA repair and mutagenesis in glioblastoma. Importantly, disruption of c-Myc/miR-29c/REV3L signalling may have dual anticancer effects, sensitizing the resistant tumours to therapy as well as preventing the emergence of acquired temozolomide resistance. Our findings suggest a rationale for targeting the c-Myc/miR-29c/REV3L signalling pathway as a promising therapeutic approach for glioblastoma, even in recurrent, treatment-refractory settings.
    No preview · Article · Oct 2015 · Brain
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    ABSTRACT: The dengue virus (DENV) envelope protein domain III (ED3) has been suggested to contain receptor recognition sites and the critical neutralizing epitopes. Up to date, relatively little work has been done on fine mapping of neutralizing epitopes on ED3 for DENV4. In this study, a novel mouse type-specific neutralizing antibody 1G6 against DENV4 was obtained with both prophylactic and therapeutic effects. The epitope was mapped to residues 387-390 of DENV4 envelope protein. Furthermore, site-directed mutagenesis assay identified two critical residues (T388 and H390). The epitope is variable among different DENV serotypes but is highly conserved among four DENV4 genotypes. Affinity measurement showed that naturally occurring variations in ED3 outside the epitope region did not alter the binding of mAb 1G6. These findings expand our understanding of the interactions between neutralizing antibodies and the DENV4 and may be valuable for rational design of DENV vaccines and antiviral drugs.
    Full-text · Article · Oct 2015 · PLoS ONE
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    ABSTRACT: We recorded motor cortical activity using high- density electrocorticogram (ECoG) from three patients during awake craniotomy. Subjects repeatedly executed hand flexion/extension tasks according to auditory instructions. Clear event-related desynchronization (ERD) in beta band (8-32) Hz and event-related synchronization (ERS) in gamma band (60-200) Hz were observed. High frequency band (HFB: 60-200 Hz) activation was found to be more localized compared to low frequency band (LFB: 8-32 Hz) activation in all subjects. Local spatial correlation maps in LFB and HFB were constructed by computing the correlation between channels. Local spatial correlation dropped more in the ERD/ERS areas consistently in two subjects. The results indicate that ERD/ERS patterns are more spatially uncorrelated and denser ECoG electrode is necessary within these areas to map uncorrelated ‘sources’. High resolution electrodes might improve both clinical functional mapping and brain machine interface outcomes in the near future.
    No preview · Conference Paper · Aug 2015
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    ABSTRACT: The goal of this work was to explore the most effective miRNAs affecting glioblastoma multiforme (GBM) phenotype transition and malignant progression. We annotated 491 TCGA samples' miRNA expression profiles according to their mRNA-based subtypes and found that the mesenchymal tumors had significantly decreased miR-181 family expression compared with the other three subtypes while the proneural subtype harbored extremely high miR-181 family expression. Patients with high miR-181 family expression had longer overall survival (p = 0.0031). We also confirmed that NF-κB-targeting genes and the EMT (epithelial-mesenchymal transition) pathway were inversely correlated with miR-181 family expression and that the entire miR-181 family inhibited glioma cell invasion and proliferation; of these, miR-181b was the most effective suppressor. Furthermore, miR-181b was validated to suppress EMT by targeting KPNA4 and was associated with survival outcome in the TCGA and CGGA datasets and in another independent cohort. The EMT-inhibitory effect of miR-181b was lost after KPNA4 expression was restored. We also identified the antitumorigenic activity of miR-181b in vitro and in vivo. Our results showed that miR-181 family expression was closely correlated with TCGA subtypes and patients' overall survival, indicating that miR-181b, a tumor-suppressive miRNA, could be a novel therapeutic candidate for treating gliomas.
    Preview · Article · Aug 2015 · Scientific Reports
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    ABSTRACT: Isorhamnetin has been reported to have anti-inflammatory, anti-oxidative, and anti-proliferative effects. The aim of this study was to investigate the protective effect of isorhamnetin on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in mice by inhibiting the expression of cyclooxygenase-2 (COX-2). The effects of isorhamnetin on LPS-induced lung pathological damage, wet/dry ratios and the total protein level in bronchoalveolar lavage fluid (BALF), inflammatory cytokine release, myeloperoxidase (MPO) and superoxide dismutase (SOD) activities, and malondialdehyde (MDA) level were examined. In addition, the COX-2 activation in lung tissues was detected by Western blot. Isorhamnetin pretreatment improved the mice survival rates. Moreover, isorhamnetin pretreatment significantly attenuated edema and the pathological changes in the lung and inhibited protein extravasation in BALF. Isorhamnetin also significantly decreased the levels of inflammatory cytokines in BALF. In addition, isorhamnetin markedly prevented LPS-induced oxidative stress. Furthermore, isorhamnetin pretreatment significantly suppressed LPS-induced activation of COX-2. Isorhamnetin has been demonstrated to protect mice from LPS-induced ALI by inhibiting the expression of COX-2.
    No preview · Article · Aug 2015 · Inflammation
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    ABSTRACT: Glioma is a most common type of primary brain tumors. Extracellular vesicles, in the form of exosomes, are known to mediate cell-cell communication by transporting cell-derived proteins and nucleic acids, including various microRNAs (miRNAs). Here we examined the cerebrospinal fluid (CSF) from patients with recurrent glioma for the levels of cancer-related miRNAs, and evaluated the values for prognosis by comparing the measures of CSF-, serum-, and exosome-contained miR-21 levels. Samples from seventy glioma patients following surgery were compared with those from brain trauma patients as a non-tumor control group. Exosomal miR-21 levels in the CSF of glioma patients were found significantly higher than in the controls; whereas no difference was detected in serum-derived exosomal miR-21 expression. The CSF-derived exosomal miR-21 levels correlated with tumor spinal/ventricle metastasis and the recurrence with anatomical site preference. From additional 198 glioma tissue samples, we verified that miR-21 levels associated with tumor grade of diagnosis and negatively correlated with the median values of patient overall survival time. We further used a lentiviral inhibitor to suppress miR-21 expression in U251 cells. The results showed that the levels of miR-21 target genes of PTEN, RECK and PDCD4 were up-regulated at protein levels. Therefore, we concluded that the exosomal miR-21 levels could be demonstrated as a promising indicator for glioma diagnosis and prognosis, particularly with values to predict tumor recurrence or metastasis.
    Preview · Article · Aug 2015 · Oncotarget

Publication Stats

6k Citations
1,386.03 Total Impact Points

Institutions

  • 2015-2016
    • Beijing Neurosurgical Institute
      Peping, Beijing, China
    • Second Military Medical University, Shanghai
      Shanghai, Shanghai Shi, China
  • 2009-2015
    • Fourth Military Medical University
      • Department of Thoracic Surgery
      Xi’an, Liaoning, China
  • 2008-2015
    • Nanjing Medical University
      • • Key Laboratory of Reproductive Medicine
      • • Department of Pediatrics
      Nan-ching, Jiangsu, China
  • 2006-2015
    • Capital Medical University
      Peping, Beijing, China
  • 2005-2015
    • Beijing Tiantan Hospital
      Peping, Beijing, China
  • 2003-2015
    • Beijing Institute of Microbiology and Epidemiology
      Peping, Beijing, China
    • Beijing Centers for Disease Control and Prevention
      Peping, Beijing, China
  • 2014
    • Beijing Shijitan Hospital
      Peping, Beijing, China
    • University of Oklahoma Health Sciences Center
      • Department of Surgery
      Oklahoma City, Oklahoma, United States
    • Chinese Academy of Sciences
      Peping, Beijing, China
    • Xinjiang Medical University
      Ouroumtchi, Xinjiang Uygur Zizhiqu, China
    • Southern Medical University
      • Department of Anesthesiology
      Shengcheng, Guangdong, China
  • 2013-2014
    • Sichuan University
      • • State Key Laboratory of Biotherapy
      • • Department of Gastroenterology and Hepatology
      Hua-yang, Sichuan, China
    • Thomas Jefferson University
      • Department of Cancer Biology
      Filadelfia, Pennsylvania, United States
  • 2012-2014
    • State Key Laboratory of Medical Genetics of China
      Ch’ang-sha-shih, Hunan, China
    • FAW Group Corporation
      Changchun, Fujian, China
  • 2006-2014
    • Harbin Medical University
      • Department of General Surgery
      Charbin, Heilongjiang Sheng, China
  • 2011-2013
    • Beijing Genomics Institute
      Bao'an, Guangdong, China
    • Shenzhen University
      Bao'an, Guangdong, China
    • University of Utah
      • Department of Psychiatry
      Salt Lake City, Utah, United States
  • 2010-2012
    • National Human Genome Research Institute
      Maryland, United States
    • Qingdao University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2009-2012
    • Shandong University of Science and Technology
      Tsingtao, Shandong Sheng, China
  • 2009-2011
    • Jilin University
      • • College of Material Science and Engineering
      • • State Key Lab of Superhard Materials
      • • Department of Material Science and Engineering
      Yung-chi, Jilin Sheng, China
  • 2005-2008
    • Academy of Military Medical Sciences
      T’ien-ching-shih, Tianjin Shi, China