Bin Zhao

Guangdong Medical College, Tsamkong, Guangdong, China

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Publications (72)221 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: To further understand the ligation mechanism, effects of 2'-O-methyl nucleotide (2'-OMeN) on the T4 DNA ligation efficiency were investigated. Fluorescence resonance energy transfer assay was used to monitor the nick-joining process by T4 DNA ligase. Results showed that substitutions at 5'- and 3'-ends of the nick decreased the ligation efficiency by 48.7 ± 6.7% and 70.6 ± 4.0%, respectively. Substitutions at both 5'- and 3'-ends decreased the ligation efficiency by 76.6 ± 1.3%. Corresponding kinetic parameters, Vmax, Km, and kcat, have been determined in each case by using the Michaelis-Menten equation. The kinetic data showed that the 2'-OMeN substitutions reduced the maximal initial velocity and increased the Michaelis constant of T4 DNA ligase. Mismatches at 5'- and 3'-ends of the nick have also shown different influences on the ligation. Results here showed that the sugar pucker conformation at 3'-end impairs the ligation efficiency more profoundly than that at 5'-end. Different concentrations of Mg(2+), Ca(2+), K(+), Na(+), and ATP were also demonstrated to affect the T4 DNA ligase activity. These results enriched our knowledge about the effects of 2'-OMeN substitutions on the T4 DNA ligase.
    Acta Biochimica et Biophysica Sinica 07/2014; · 1.81 Impact Factor
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    ABSTRACT: Parkinson's disease (PD) drug therapy remains a challenge. Dual modulation of dopamine and 5-HT receptors has emerged as a promising approach in anti-PD drug development. Taking advantage of the newly discovered aporphine analogue(s), (6aR)-11-amino-N-propyl-noraporphine (SOMCL-171), which exhibited dual D2/5-HT1A receptor agonistic activity, we studied the effects of the compound on levodopa-induced dyskinesia (LID) in a PD animal model. The results demonstrated that SOMCL-171 elicited a potent anti-PD effect in a 6-OHDA-lesioned rat model. Chronic use of SOMCL-171 reduced LID without compromising the antiparkinsonian efficacy. Furthermore, we found that the antidyskinesia effect of SOMCL-171 is associated with its 5-HT1A agonistic activity and the up-regulation of the striatal 5-HT1A receptor. The present data indicated that chronic SOMCL-171 alone produced potent antiparkinsonian effects with weak dyskinesia, compared with that of levodopa. In addition, chronic SOMCL-171 application attenuated the development of levodopa-induced LID at no expense to the antiparkinsonian efficacy. Taken together, our data suggested that dual modulation of D2/5-HT1A receptors may provide a novel approach for drug development in PD and LID.
    Pharmacology Biochemistry and Behavior 06/2014; · 2.61 Impact Factor
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    ABSTRACT: The complement receptor 1 (CR1) rs6656401 polymorphism was first identified to be associated with Alzheimer's disease (AD) in European ancestry. However, the following studies reported weak or no significant association in Chinese, Japanese, Korean, African-American, Polish, and Canadian populations. We think that these negative results may have been caused by either relatively small sample sizes compared with those used for the previous genome-wide association studies (GWAS) in European ancestry or the genetic heterogeneity of the rs6656401 polymorphism in different populations. Here, we reevaluated this association using the relatively large-scale samples from previous 24 studies (N = 85,939, 30,100 cases and 55,839 controls) by searching the PubMed, AlzGene, and Google Scholar databases. Using additive model, we did not identify significant heterogeneity among the 24 studies. We observed significant association between the rs6656401 polymorphism and AD in pooled populations (P = 1.82E-26, odds ratio (OR) = 1.18, 95 % confidence interval (CI) 1.15-1.22). In subgroup analysis, we identified significant results in East Asian population with P = 5.00E-04, OR = 1.31, 95 % CI 1.13-1.52. To our knowledge, this is the first meta-analysis to investigate the association between rs6656401 polymorphism and AD in East Asian, African-American, Canadian, and European populations. Our analysis further supports previous findings that the CR1 rs6656401 polymorphism contributes to AD susceptibility. We believe that our findings will be very useful for future genetic studies on AD.
    Molecular neurobiology. 05/2014;
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    ABSTRACT: Atherosclerosis is the leading etiologic factor of Atherosclerotic Cerebral Infarction (ACI). Previous studies have shown that thrombin activatable fibrinolysis inhibitor (TAFI) may play an important role in the occurrence of acute cerebral infarction, and the levels of TAFI are affected by several single nucleotide polymorphisms (SNPs) located in the regulatory and coding regions of the gene encoding TAFI. The present study aimed to determine whether polymorphisms (TAFI -2345 2G/1G, -1690 A/G, -438 A/G, +1583 A/T) of the TAFI gene were associated with ACI in a Han Chinese population.
    Lipids in Health and Disease 05/2014; 13(1):80. · 2.02 Impact Factor
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    ABSTRACT: Background: Accumulating evidence suggests that the principal TNF-α converting enzyme, a disintegrin and metalloproteinase 17 (ADAM17), is involved in the development of human abdominal aortic aneurysm (AAA). However, the association between ADAM17 gene polymorphisms and AAA has not been explored. The present study was aimed to determine the association between ADAM17 promoter polymorphisms and AAA. Methods: A total of 316 patients with AAA and 306 age-matched healthy controls were enrolled in this study. Two ADAM17 promoter polymorphisms (rs12692386 and rs1524668) were determind. Real-time PCR was employed to detect the expression of ADAM17. Results: Overall, there was a significant difference in the frequency of the genotype rs12692386 between the AAA and control subjects (P=0.0096). Furthermore, men with the rs12692386 AG genotype conferred a higher risk of developing AAA (P=0.0058). Additionally, the rs12692386 mutated AG genotype of ADAM17 was significantly associated with increased ADAM17 expression (P=0.035) and TNF-α production (P=0.042) in AAA patients. In contrast, the allele frequency of rs1524668 was not statistically associated with AAA. Conclusions: Our findings indicate a positive association between the rs12692386 polymorphism of ADAM17 and AAA. This new knowledge about ADAM17 identifies a role for ADAM17 in the pathophysiology of AAA and has important clinical implications with regard to potential therapeutics. © 2014 S. Karger AG, Basel.
    05/2014; 33(5):1426-1438.
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    ABSTRACT: Aim: Stroke is a leading cause of death and disability worldwide. Most ischemic strokes (IS) are caused by atherosclerosis. Recently, the pivotal role of ADAM17 in atherosclerosis has been thoroughly addressed. However, the association between ADAM17 and IS has not yet been thoroughly explored. The present study therefore aimed to investigate the association between disintegrin and metalloproteinase 17 (ADAM17) gene polymorphisms and the risk of ischemic stroke (IS). Methods: The associations between five ADAM17 promoter polymorphisms and the risk of IS were assessed in 342 patients with IS and 296 age-matched healthy individuals in a case-control study. Results: The allele and genotype frequencies of the ADAM17 polymorphisms (rs11684747, rs11689958, rs12692386, rs55790676 and rs1524668) did not differ significantly between the IS patients and healthy control group subjects. In addition, no significant associations were detected between the ADAM17 haplotypes and IS. The mean intima-media thickness in the IS patients was not associated with the ADAM17 polymorphisms. When the IS patients were stratified according to their OCSP classification, the genotype frequencies of the ADAM17-rs1524668 polymorphism exhibited a significant association with the PACI subtype of IS. Moreover, the ADAM17-rs12692386 A>G polymorphism was found to be associated with a higher ADAM17 mRNA expression. Conclusions: The SNPs in the ADAM17 promoter region do not appear to be major contributors to the pathogenesis of IS. However, the rs12692386 G ADAM17 allele is correlated with a higher expression of ADAM17 mRNA, which may play a role in increasing inflammation in IS patients. Furthermore, the ADAM17-rs1524668 polymorphism is linked to a higher risk of PACI-type stroke, confirming the role of ADAM17 in the pathophysiology of PACI, with potentially important therapeutic implications.
    Journal of atherosclerosis and thrombosis 04/2014; · 2.93 Impact Factor
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    ABSTRACT: Large-scale genome-wide association studies (GWAS) have revealed that the ABCA7 rs3764650 polymorphism (or its proxies, namely rs115550680, rs3752246, and rs4147929) is associated with Alzheimer's disease (AD) susceptibility in individuals of Caucasian ancestry. The following studies have investigated this finding in Chinese (N = 633 and N = 1,224), Japanese (N = 1,735), Korean (N = 844), African American (N = 5,896), and Canadian (N = 1,104) populations. However, these studies reported a weak or negligible association. We hypothesized that these negative results may have been caused by either relatively small sample sizes compared with those used for the previous GWAS in individuals of Caucasian ancestry or the genetic heterogeneity of the rs3764650 polymorphism (or its proxies) in different populations. Here, we reevaluated the association between rs3764650 and AD using large-scale samples from 18 previous studies (N = 79,381-30,590 cases and 48,791 controls) by searching PubMed, AlzGene, and Google Scholar databases. Using allele, dominant, recessive, and additive models, we did not identify significant heterogeneity among the 18 studies. We observed a significant association between rs3764650 and AD using the allele (P = 1.76E - 26, odds ratio (OR) = 1.21, 95 % confidence interval (CI) 1.17-1.26), dominant (P = 4.00E - 04, OR = 1.17, 95 % CI 1.07-1.28), recessive (P = 3.00E - 03, OR = 1.43, 95 % CI 1.13-1.81), and additive models (P = 3.00E - 03, OR = 1.49, 95 % CI 1.16-1.91). Collectively, our analysis further supports previous findings that the ABCA7 rs3764650 polymorphism is associated with AD susceptibility. We believe that our findings will be very useful for future genetic studies on AD.
    Molecular Neurobiology 03/2014; · 5.47 Impact Factor
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    ABSTRACT: Autophagy eliminates dysfunctional mitochondria in an intricate process known as mitophagy. ULK1 is critical for the induction of autophagy, but its substrate(s) and mechanism of action in mitophagy remain unclear. Here, we show that ULK1 is upregulated and translocates to fragmented mitochondria upon mitophagy induction by either hypoxia or mitochondrial uncouplers. At mitochondria, ULK1 interacts with FUNDC1, phosphorylating it at serine 17, which enhances FUNDC1 binding to LC3. A ULK1-binding-deficient mutant of FUNDC1 prevents ULK1 translocation to mitochondria and inhibits mitophagy. Finally, kinase-active ULK1 and a phospho-mimicking mutant of FUNDC1 rescue mitophagy in ULK1-null cells. Thus, we conclude that FUNDC1 regulates ULK1 recruitment to damaged mitochondria, where FUNDC1 phosphorylation by ULK1 is crucial for mitophagy.
    EMBO Reports 03/2014; · 7.19 Impact Factor
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    ABSTRACT: Mitophagy receptors mediate the selective recognition and targeting of damaged mitochondria by autophagosomes. The mechanism for the regulation of these receptors remains unknown. Here, we demonstrated that a novel hypoxia-responsive microRNA, microRNA-137 (miR-137), markedly inhibits mitochondrial degradation by autophagy without affecting global autophagy. MiR-137 targets the expression of two mitophagy receptors NIX and FUNDC1. Impaired mitophagy in response to hypoxia caused by miR-137 is reversed by re-expression of FUNDC1 and NIX expression vectors lacking the miR-137 recognition sites at their 3' UTR. Conversely, miR-137 also suppresses the mitophagy induced by FUNDC1 (CDS+3'UTR) but not FUNDC1 (CDS) overespression. Finally, we found that miR-137 inhibits mitophagy by reducing the expression of the mitophagy receptor thereby leads to inadequate interaction between mitophagy receptor and LC3. Our results demonstrated the regulatory role of miRNA to mitophagy receptors and revealed a novel link between miR-137 and mitophagy.
    Journal of Biological Chemistry 02/2014; · 4.65 Impact Factor
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    ABSTRACT: The receptor for advanced glycation end products (RAGE) is a cell surface molecule of the immunoglobulin superfamily that binds diverse endogenous ligands involved in the development of chronic diseases and inflammatory damage. A growing body of evidence has suggested that RAGE is involved in the development and progression of chronic obstructive pulmonary disease (COPD). The present study investigated the existence of an association among three polymorphisms (-374T/A, -429T/C, and G82S) of the RAGE gene with the risk of COPD in the Chinese population. The RAGE genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism in 216 patients with COPD and 239 age-matched healthy individuals. Our study demonstrated that the frequencies of the GS genotype and the S allele in the G82S mutation were significantly higher in COPD patients than in controls (odds ratios [OR]=1.70, 95% confidence interval [CI]: 1.15-2.50, p=0.0098 and OR=1.42, 95% CI: 1.06-1.91, p=0.023, respectively). Further stratification analysis by smoking status revealed that the presence of the GS genotype conferred a higher risk of developing COPD in current smokers (p=0.044). In contrast, mutations at -374T/A and -429T/C did not demonstrate any association with COPD, even after taking into account the patients' smoking history. Our study provides preliminary evidence that the G82S polymorphism in the RAGE gene is associated with an increased risk of COPD and that the GS genotype of the G82S variant is a risk factor for COPD in the Chinese population.
    DNA and cell biology 02/2014; · 2.28 Impact Factor
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    ABSTRACT: Angiotensin (Ang) II exaggerates cerebral injury in ischemic damage. Angiotensin-converting enzyme type 2 (ACE2) converts Ang II into Ang (1-7) and thus, may protect against the effects of Ang II. We hypothesized that neuronal ACE2 over-expression decreases ischemic stroke in mice with Ang II overproduction. Human renin and angiotensinogen double transgenic (RA) mice and RA mice with neuronal over-expression of ACE2 (SARA) were used for the study. The mean arterial pressure (MAP) was calculated from telemetry-recorded blood pressure (BP). SARA mice were infused peripherally with Norepinephrine to "clamp" the BP, or intracerebroventricularly-infused with a Mas receptor antagonist (A-779). Middle cerebral artery occlusion (MCAO) surgery was performed to induce permanent focal ischemic stroke. Cerebral blood flow (CBF) and neurological function were determined. Two days after surgery, brain samples were collected for various analyses. Results showed: 1) When compared to chronically hypertensive RA mice, SARA mice had lower basal MAP, less MCAO-induced infarct volume, and increased CBF, neurological function and cerebral microvascular density in the peri-infarct area; 2) These changes in SARA mice were not altered after MAP "clamping", but partially reversed by brain infusion of A-779; 3) Ang (1-7)/Ang II ratio, angiogenic factors, endothelial nitric oxide synthase (eNOS) expression and nitric oxide production were increased, whereas, NADPH oxidase subunits and reactive oxygen species were decreased in the brain of SARA mice. ACE2 protects brain from ischemic injury via the regulation of NADPH oxidase/eNOS pathways by changing Ang (1-7)/Ang II ratio, independently of MAP changes.
    Neuropharmacology 01/2014; · 4.11 Impact Factor
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    ABSTRACT: miR146a is well known for its regulatory role in the immune response and inflammation. Recent studies have demonstrated the links between miR146a and Alzheimer disease (AD) and suggested that miR146a may be involved in neuroinflammation and the metabolism of amyloid-β (Aβ), which are critical events in AD pathology. Although genetic studies have focused on the association between the miR146a gene and susceptibility to several diseases, no association study of miR146a variability with AD has been conducted. In this report, we performed a case-control association study to analyze the genotype and allele distributions of the miR146a, rs2910464 and rs57095329 polymorphisms in a Chinese population consisting of 292 AD cases and 300 healthy controls. We found a significant difference in the genotypes and allele frequencies of rs57095329 between the AD cases and the controls (p = 0.0147 and p = 0.0184, respectively), where the AA genotype of rs57095329 was associated with an increased risk of AD as well the cognitive decline in AD patients. Additionally, the AA genotype of rs57095329 exhibited significantly higher miR146a expression than the GG+GA genotypes of rs2910164 in the peripheral blood cells (PBMCs) of healthy individuals and had a stronger effect on the production of IL-6 and IL-1β when the cells were stimulated with LPS. Our data provide preliminary evidence that the rs57095329 polymorphism in the miR146a promoter is involved in the genetic susceptibility to AD, and this risk AA genotype may increase the expression of miR146a and influence certain proinflammatory cytokines, thus playing a role in the pathogenesis of AD.
    PLoS ONE 01/2014; 9(2):e89019. · 3.73 Impact Factor
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    ABSTRACT: Co3O4/graphene nanosheet (GNS) composites were synthesized via the in situ growth of mesoporous Co3O4 nanoparticles on graphene. The as-prepared Co3O4/GNS composites exhibited superior Li-ion battery performance and showed a large reversible capacity, excellent cycling, and good rate capability when used as an anode material in lithium ion batteries (LIBs). The uniform coating of Co3O4 around the graphene surface ensured tight electrical contact, resulting in a material with higher specific capacity and enhanced cycling performance compared with pure Co3O4 electrodes. The composites delivered a reversible capacity of 900 mA h g−1 at a discharge current density of 100 mA g−1 with good cycling ability. Moreover, the composites showed exceptional high-current charge–discharge performance, achieving 650 mA h g−1 at a current density of 1000 mA g−1.
    Materials Letters. 01/2014; 119:12–15.
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    ABSTRACT: MicroRNA-146a (miR-146a) acts as a pivotal regulatory molecule in immune response and various diseases, such as carcinoma and autoimmune diseases. Growing evidences have demonstrated the association of miR-146a gene single-nucleotide polymorphisms (SNPs) with risk of several diseases, but no genetic relevance studies of miR-146a gene polymorphisms to sepsis have been reported by now. Our study has analyzed the association of sepsis with two functional miR-146a gene SNPs rs2910164 G/C and rs57095329 A/G in a Chinese Han population (226 sepsis cases; 206 healthy controls). Our results indicated a higher prevalence of the miR-146a gene SNP rs2910164 C allele and CC genotype in patients with severe sepsis (rs2910164G versus rs2910164C: P = 0.0029, odds ratio (OR) = 1.664; GG+GC versus CC: P = 0.0045, OR = 1.947). Neither the genotype nor the allele in rs57095329 showed significant differences between the septic cases and the controls (P = 0.5901 and 0.3580, resp.), and no significant difference was observed in the subgroups. In addition, we confirmed that the two SNPs rs2910164 and rs57095329 could functionally affect the miR-146a expression levels and the reduction of miR146a was accompanied with the upregulation of the expression levels of TRAF-6 and IRAK-1 in severe sepsis patients. This present study might provide valuable clinical evidence that miR-146a gene polymorphism rs2910164 is associated with the risk of severe sepsis.
    Mediators of Inflammation 01/2014; 2014:916202. · 3.88 Impact Factor
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    ABSTRACT: The HIV-1 epidemic among men-who-have-sex-with-men (MSM) continues to expand in China. A large-scale national survey we conducted on HIV-1 strains among MSM in 11 provinces in China from 2008 to 2013 (n = 920) identified a novel transmission cluster consisting of six strains (0.7%) that belonged to a new circulating recombinant form (designated CRF59_01B). CRF59_01B contains two subtype B segments of U.S.-European origin (in the pol and vpu-env regions) in a CRF01_AE backbone. CRF59_01B is the second CRF (after CRF55_01B) circulating primarily among MSM in China. CRF59_01B occurs at a low frequency (less than 1%), but it was detected in four different provinces/regions in China: Liaoning (northeast China) (n = 3); Hunan (central China) (n = 1); Guangdong (south China) (n = 1); Yunnan (southwest China) (n = 1). One additional recombinant strain was detected in a heterosexual individual in Liaoning province but is not the focus of this paper. Bayesian molecular clock analyses indicate that CRF59_01B emerged as a result of recombination between CRF01_AE and subtype B around the year 2001. The emergence of multiple forms of recombinants and CRFs reflects the ever-increasing contribution of homosexual transmission in China's HIV epidemic and indicates an active HIV transmission network among MSM in China.
    PLoS ONE 01/2014; 9(6):e99693. · 3.73 Impact Factor
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    ABSTRACT: Alzheimer's disease (AD) is the most common and complex neurodegenerative disease in the elderly individuals. Recently, genome-wide association studies (GWAS) have been used to investigate AD pathogenesis. These GWAS have yielded important new insights into the genetic mechanisms of AD. However, these newly identified AD susceptibility loci exert only very small risk effects and cannot fully explain the underlying AD genetic risk. We hypothesize that combining the findings from different AD GWAS may have greater power than genetic analysis alone. To identify new AD risk factors, we integrated findings from 3 previous large-scale AD GWAS (n = 14,138) using a gene-based meta-analysis and subsequently conducted a pathway analysis using the kyoto encyclopedia of genes and genomes and gene ontology databases. Interestingly, we not only confirmed previous findings, but also highlighted, for the first time, the involvement of cardiovascular disease-related pathways in AD. Our results provided the clues as to the link between these diseases using pathway analysis methods. We believe that these findings will be very useful for future genetic studies of AD.
    Neurobiology of Aging. 01/2014; 35(4):786–792.
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    ABSTRACT: Myostatin, a member of the TGF-β superfamily, has been shown to act as a negative regulator of myogenesis. Although its role in myogenesis has been clearly documented through genetic analysis, few gene cascades that respond to myostatin signaling and regulate myogenesis have been characterized, especially in avian species. In a previous study, we screened for such genes in chicken fetal myoblasts (CFMs) using the differential display PCR method and found that cardiac ankyrin repeat protein (CARP) was downregulated by myostatin and specifically expressed in chicken skeletal muscle. However, little is known about the potential functions of CARP in chicken skeletal myogenesis. In this study, the expression patterns of chicken CARP and the possible function of this gene in skeletal muscle growth were characterized. Our data showed that CARP was predominantly expressed in postnatal skeletal muscle, and its expression increased during myogenic differentiation in CFM cells. When CARP was overexpressed, CFM cell growth was enhanced by accelerating the cell cycle at the G1 to S phase transition and increasing cyclin D1 expression. CARP knockdown had the opposite effect: while myoblasts underwent differentiation, knockdown of CARP expression induced extensive cell death, suppressed the formation of myotubes, and markedly decreased the expression of differentiation-related genes such as myosin heavy chain (MHC), myoD, and caveolin-3. Our findings indicate that CARP may play a key role in the myostatin signaling cascade that governs chicken skeletal myogenesis through promoting proliferation and avoiding apoptosis during CFM cell differentiation.
    International journal of biological sciences 01/2014; 10(3):309-320. · 3.17 Impact Factor
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    ABSTRACT: Fe2O3 nanocrystals were uniformly anchored onto graphene nanosheets (Fe2O3@GNS) by a nanocasting technique, and the resulting composites were applied as anodes of sodium-ion batteries. Fe2O3@GNS exhibits excellent cycling performance and rate capability.
    Chemical Communications 12/2013; · 6.38 Impact Factor
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    ABSTRACT: Background The translationally controlled tumor protein (TCTP) is a multifunctional protein that plays important roles in immune responses, cell proliferation, tumorigenicity and cell apoptosis. Here, we examined the clinical value of TCTP in glioma patient survival and investigated the functional roles and mechanism of TCTP in glioma development.MethodsTCTP expression was determined through immunohistochemical staining, immunoblotting, and quantitative real-time PCR (qRT-PCR). TCTP or TCF-4 expression was silenced using short hairpin (sh) RNA. In vitro cell proliferation was detected using MTT, BrdU and colony formation assays, and in vivo tumor growth was performed using the xenograft model. TCTP/TCF-4/β-catenin association was detected using a co-immunoprecipitation (co-IP) assay. TCF-4 transcription activity was detected using a TOPflash/FOPflash report gene assay. Wnt/β-catenin-targeted gene expression was detected through Western blotting.ResultsTCTP protein levels were significantly elevated in high-grade gliomas compared with low-grade gliomas and normal brain tissues. Importantly, the expression of TCTP was significantly associated with poorer overall survival and disease-free survival, and TCTP also reduced the survival rate after treatment with radiotherapy and temozolomide (RT-TMZ) for glioma patients. The ectopic expression of TCTP enhanced glioma cell proliferation both in vitro and in vivo, whereas the knockdown of TCTP inhibited this effect. Similarly, the overexpression of TCTP increased β-catenin binding to TCF-4, TOPflash report gene transcription activity, and the expression of Wnt/β-catenin signaling target genes including c-Myc and cyclin D1; notably, the knockdown of TCTP reduced these effects. The knockdown of TCF-4 using shRNA rescued the enhanced cell proliferation induced by the overexpression of TCTP.ConclusionTCTP is associated with reduced survival of glioma patients and induces glioma tumor growth through enhanced Wnt/β-catenin signaling.
    Neuro-Oncology 12/2013; · 6.18 Impact Factor
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    ABSTRACT: Alzheimer's disease (AD) is the most common and complex neurodegenerative disease in the elderly individuals. Recently, genome-wide association studies (GWAS) have been used to investigate AD pathogenesis. These GWAS have yielded important new insights into the genetic mechanisms of AD. However, these newly identified AD susceptibility loci exert only very small risk effects and cannot fully explain the underlying AD genetic risk. We hypothesize that combining the findings from different AD GWAS may have greater power than genetic analysis alone. To identify new AD risk factors, we integrated findings from 3 previous large-scale AD GWAS (n = 14,138) using a gene-based meta-analysis and subsequently conducted a pathway analysis using the kyoto encyclopedia of genes and genomes and gene ontology databases. Interestingly, we not only confirmed previous findings, but also highlighted, for the first time, the involvement of cardiovascular disease-related pathways in AD. Our results provided the clues as to the link between these diseases using pathway analysis methods. We believe that these findings will be very useful for future genetic studies of AD.
    Neurobiology of aging 10/2013; · 5.94 Impact Factor

Publication Stats

213 Citations
221.00 Total Impact Points

Institutions

  • 2012–2014
    • Guangdong Medical College
      Tsamkong, Guangdong, China
    • Nanjing University
      • School of Electronic Science & Engineering
      Nan-ching, Jiangsu Sheng, China
    • China Earthquake Administration
      Peping, Beijing, China
  • 2013
    • Southern Medical University
      Shengcheng, Guangdong, China
  • 2011–2013
    • Wright State University
      • Department of Pharmacology and Toxicology
      Dayton, Ohio, United States
    • Guangzhou First People's Hospital
      Shengcheng, Guangdong, China
  • 2010–2013
    • China Medical University (PRC)
      • Key Laboratory of AIDS Immunology, Ministry of Health
      Shenyang, Liaoning, China
    • Northeast Institute of Geography and Agroecology
      • State Key Laboratory of Drug Research
      Peping, Beijing, China