Jinghui Zhang

Huazhong University of Science and Technology, Wu-han-shih, Hubei, China

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Publications (11)18.71 Total impact

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    ABSTRACT: People with type 2 diabetes (T2DM) mellitus are high risk for dementia and Alzheimer's disease (AD) via several plausible pathways. However, the underlying mechanisms have been still unclear, and the relation of immune injury to the pathogenesis of T2DM-related AD is not yet completely understood. Our present study aimed to elucidate the possible role of immunoglobulin IgG in the immune process of AD associated with T2DM in db/db mice. Hippocampi of 20 db/db mice and 20 C57BL/6 mice were subjected to immunohistochemistry and immunofluorescence assays. The phosphorylation of tau, glycogen synthase kinase (GSK)-3β and AKT activity was examined by Western blot analysis. IgG purified from the sera of IgG deposit-positive db/db mice was stereotaxically injected into the hippocampi of another 12 db/db mice and 12 C57BL/6 mice. The phosphorylation of tau, Abeta, GSK-3β and AKT activity was analyzed. Compared with the C57BL/6 control, 13 of the 20 db/db mice exhibited high levels of IgG deposits in the hippocampus. Treatment with IgG triggered tau hyperphosphorylations and Abeta deposition, which are likely major factors in AD. Meanwhile, IgG inhibited AKT phosphorylation and promoted GSK-3β activity. The IgG deposits observed in some db/db mice were possibly related to the impairment of T2DM-related AD development. Some autoimmune processes may be involved in AD in type 2 diabetes mellitus development at the level of the hippocampus.
    Brain research 10/2012; 1486. DOI:10.1016/j.brainres.2012.08.049 · 2.83 Impact Factor
  • Jinbo Gao · Yuan Tian · Jinghui Zhang
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    ABSTRACT: To investigate the effects of interferon regulatory factor 1 (IRF-1) gene overexpression on chemotherapeutic sensitivity of gastric cancer cells. An AGS cell system with tetracycline-inducible IRF-1 expression (AGS/IRF-1) was established. Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting were used to detect the expression of the IRF-1 gene. Chemosensitivity to 5-fluorouracil (5-FU) was assessed by cell proliferation assay and cell apoptosis. IRF-1 mRNA and protein level were significantly increased in AGS/IRF-1 cells induced with tetracycline. Compared with control cells, the growth inhibition rate of cells with IRF-1 overexpression was significantly increased when treated with 5-FU (P<0.01). Treatment with 5 μmol/l 5-FU resulted in 12.6% apoptotic cells, whereas such treatment after overexpression of IRF-1 resulted in 39.4% apoptotic cells. Moreover, more poly(adenosine diphosphate-ribose) polymerase (PARP) cleavage was seen in cells with IRF-1 overexpression. Overexpression of IRF-1 enhanced the chemosensitivity of gastric cancer cells to 5-FU through induction of apoptosis.
    Journal of cancer research and therapeutics 01/2012; 8(1):57-61. DOI:10.4103/0973-1482.95175 · 0.95 Impact Factor
  • Jinbo Gao · Jinghui Zhang · Yaoping Long · Xiaoming Lu
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    ABSTRACT: The aim of this study was to investigate the expression of telomere repeat binding factor 1 (TRF1), TRF2 and protection of telomeres 1 (POT1) in gastric cancer and their relationships with clinicopathological features and telomerase activity. In total 36 gastric cancer tissue and paired adjacent normal tissue were analyzed. The mRNA expression of telomere binding proteins TRF1, TRF2 and POT1 were measured using quantitative reverse transcription polymerase chain reaction, and telomerase activity was assessed by the telomeric repeat amplification protocol/enzyme linked immunosorbent assay method. The expression of POT1 was significantly higher in tumor tissue than in adjacent normal tissue (P < 0.001). Levels of TRF2 mRNA were significantly higher in bigger tumors (diameter ≥ 5 cm) than in small tumors (diameter < 5 cm) (P = 0.043). POT1 mRNA transcription levels were higher in tumors with lymph nodes metastases than in those without lymph nodes metastases (P = 0.048). POT1 expression was significantly correlated with tumor stage (P = 0.008). A higher level of expression of POT1 was observed in late-stage tumors (III, IV) than in early stage tumors (I, II). Telomerase activity was significantly higher in gastric cancers than in corresponding normal tissue (P < 0.001). Moreover, POT1 expression was significantly positive correlated with telomerase activity (r = 0.572, P < 0.01). POT1 was overexpressed in gastric cancer and may be associated with stomach carcinogenesis and gastric cancer progression.
    Asia-Pacific Journal of Clinical Oncology 12/2011; 7(4):339-45. DOI:10.1111/j.1743-7563.2011.01437.x · 1.06 Impact Factor
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    ABSTRACT: Hypoxia is a critical event in solid tumor development, invasion, and metastasis. Cellular adaptation to hypoxic microenvironment is essential for tumor progression and is largely mediated by hypoxia-inducible factor-1α (HIF-1α) through coordinated regulation of hypoxia-responsive genes. In this study, we found that membrane type-2 matrix metalloproteinase (MT2-MMP), one of the matrix metalloproteinase (MMP) family members, was a novel hypoxia-responsive gene and was upregulated by HIF-1α under hypoxia. When cancer cells were subjected to hypoxia (1% O(2) ) treatment, the mRNA and protein levels of MT2-MMP were significantly increased in a time-dependent manner in all three tested cancer cell lines including pancreatic cancer cells (PANC-1), nonsmall cell lung cancer cells (A-549), and cervix cancer cells (HeLa). Further analyses indicated that there were two hypoxia-responsive elements (HREs) in the MT2-MMP promoter, and HRE1 but not HRE2 was essential for MT2-MMP transcriptional activation under hypoxia. HIF-1α specifically and directly bound to MT2-MMP promoter was analyzed by HIF-1α binding/competition and chromatin immunoprecipitation (ChIP) assays. Furthermore, we found that upregulation of MT2-MMP under hypoxia could confer resistance to hypoxia-induced apoptosis and increase invasiveness of cancer cells. These findings provided a new insight into how cancer cells overcome hypoxic stress and trend to survive and invade, demonstrated a new regulatory mechanism of MT2-MMP expression in caner cells, and also revealed that MT2-MMP was a novel hypoxia-responsive gene and was upregulated by HIF-1α under hypoxia. © 2011 Wiley-Liss, Inc.
    Molecular Carcinogenesis 10/2011; 50(10):770-80. DOI:10.1002/mc.20678 · 4.77 Impact Factor
  • Jinbo Gao · Jinghui Zhang · Yaoping Long · Yuan Tian · Xiaoming Lu
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    ABSTRACT: Tankyrase 1, which enhances telomerase access to telomeres, plays an important role in telomere maintenance. The aim of this study was to determine the expression and potential role of tankyrase 1 in gastric cancer development and progression. We examined the expression of tankyrase 1 by RT-PCR and Western blotting, and assessed telomerase activity by TRAP-ELISA method in gastric cancer and adjacent normal tissues. We found that tankyrase 1 expression was significantly up-regulated in gastric cancer tissues compared to normal corresponding tissues. Tankyrase 1 over-expression by gastric cancerous tissue was significantly associated with tumor histology differentiation and tumor stage. Moreover, tankyrase 1 expression was significantly correlation with telomerase activity. Our results indicate that tankyrase 1 over-expression may play an important role in gastric cancer development and progression. Tankyrase 1 may be used as a biomarker of gastric cancer and may serve as a target for cancer therapy.
    Pathology & Oncology Research 04/2011; 17(3):685-90. DOI:10.1007/s12253-011-9369-8 · 1.81 Impact Factor
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    ABSTRACT: Erythropoietin (EPO) is a cytokine that regulates the proliferation, differentiation, and survival of erythroid progenitor cells. EPO has recently been demonstrated to have a tissue-protective role by mediating anti-apoptotic signals through the erythropoietin receptor (EPOR) in various tissues, including brain, liver, and heart. We have previously examined pancreatic β-cell line NIT-1 cells for the expression of EPOR by real-time PCR and determined that these cells were protected by EPO against cytokine-induced apoptosis. The precise underlying anti-apoptotic mechanisms in pancreatic β-cells are poorly understood. The purpose of this study is to examine erythropoietin receptor expression in the NIT-1 pancreatic beta-cell line and the intracellular pathway related with its anti-apoptosis effect in NIT-1 cells. we examined the expression of EPOR by western blot. We investigate the role of erythropoietin in the survival of these cells, and whether the PI3K/AKT pathway is involved in this protective process. NIT-1 cells expressed EPOR and, in the presence of certain cytokines, exposure of NIT-1 cells to recombinant human erythropoietin (rhEPO) significantly improved the impaired insulin secretion and inhibited cytokine-induced apoptosis. RhEPO caused a rapid activation of Akt and increased expression of Bcl-2. The protective anti-apoptotic effect of rhEPO was significantly abolished by a specific phosphatidylinositol 3-kiniase (PI3K) inhibitor, LY294002. Our findings indicate that EPOR is expressed in pancreatic β-cell line NIT-1 cells and suggest that EPO may act as a survival factor requiring the PI3K/Akt pathway.
    Endocrine Research 01/2011; 36(1):25-34. DOI:10.3109/07435800.2010.534753 · 1.41 Impact Factor
  • Peng Sun · Qing Zhang · JiYuan Han · Yuan Tian · JingHui Zhang
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    ABSTRACT: Both TLR4 and TLR2 participated in the mediation of the inflammatory injury in the process of partial cerebral ischemia/reperfusion. However, it still remains unclear whether a crosstalk exists between TLR2 and TLR4 in ischemic cerebral damage. In the present study, we investigated the effect of TLR4 signaling on TLR2 expression during mimic cerebral I/R in vitro. BV-2 cells were cultured and treated with ischemia/reperfusion, then transfected with the plasmid pEGFP-H1/TLR4-siRNA, the plasmid pEGFP-H1/control sequence-siRNA and the blank plasmid, respectively. Interestingly, the expression of TLR2 and TLR4 mRNA and protein, NF-kappaB p65 mRNA and supernatant TNF-alpha level were significantly higher in ischemia/reperfusion treated cells than those lack of ischemia/reperfusion treatment, and as compared with those in ischemia/reperfusion treated cells without transfection, no significant differences about the above mentioned gene and protein expression were found in the blank plasmid tranfected cells and the plasmid pEGFP-H1/control sequence-siRNA transfected cells respectively, while the expression levels in the plasmid pEGFP-H1/TLR4-siRNA transfected cells were significantly lower. Additionally, in order to determine the effects of pyrrolidinediethyldithiocarbamate (PDTC), an NF-kappaB inhibitor, on the TLR4-induced TLR2 expression in BV-2 cells treated with ischemia/reperfusion, it was found that TLR4 and TLR2 mRNA expressions in PDTC pretreated cells were significantly lower in comparison with normal saline pretreated cells and non-pretreated cells. The data suggested that TLR2 activation, signaled by TLR4 and regulated by NF-kappaB, might be directly involved play an important role in ischemia/reperfusion induced brain damage.
    Science China. Life sciences 02/2010; 53(2):223-8. DOI:10.1007/s11427-010-0047-y · 1.51 Impact Factor
  • Shu Wang · Jing Liu · Min Wang · Jinghui Zhang · Zhaohui Wang
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    ABSTRACT: Experimental autoimmune myocarditis (EAM), a rodent model of human dilated cardiomyopathy (DCM), is mediated by an autoimmune mechanism. We investigated whether a CD28 superagonistic antibody selectively targeting CD4+CD25+ regulatory T cells (T(regs)) provides effective therapy for EAM. Four groups of 5 rats were used. The normal control group was immunized with PBS. The EAM group was immunized with porcine myosin. The experimental group was immunized with myosin and superagonistic CD28 antibody JJ316. The final group was immunized with myosin and an unrelated rat IgG. Autoantibody and IL-10 production, CD4+CD25+ cell levels, Foxp3 expression and cardiac histology were analyzed. Anti-myosin autoantibody levels were higher in the EAM and isotype control groups than the normal control group (p < 0.05), and reduced in the CD28-JJ316 group (p < 0.05). The levels of CD25+CD4+ cells, IL-10 and splenocyte Foxp3 expression were significantly lower in the EAM and isotype control groups versus the CD28-JJ316 group (p < 0.05). Infiltration of inflammatory cells was observed in the EAM and isotype control groups, whereas CD28-JJ316 ameliorated myocarditis. CD28 superagonists could be effective in EAM treatment by up-regulating Foxp3 expression and contributing to CD4+CD25+ T(reg) activation and expansion. The enhancement in IL-10 by CD28 superagonists also ameliorated the disease.
    Cardiology 11/2009; 115(2):107-13. DOI:10.1159/000256660 · 2.04 Impact Factor
  • Qing Zhang · Peng Sun · Shihai Zhang · Yuan Tian · Jinghui Zhang
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    ABSTRACT: This study investigated the effects of propofol on the mRNA expression of Toll-like receptor-4 (TLR4) in BV-2 cells during mimic ischemia-reperfusion (I/R) injury in vitro. BV-2 cells, a mouse microglia line, were cultured and divided into 4 groups at random: control group (group C), ischemia/reperfusion group (group I/R), low-dose propofol (25 micromol/L) intervention group (group PF(25)) and high-dose propofol (100 micromol/L) intervention group (group PF(100)). The mRNA expression of TLR4 and NF-kappaB was measured by means of RT-PCR. TNF-alpha levels in the supernatants of BV-2 cells were detected by ELISA. The results showed that the mRNA expression of TLR4 and NF-kappaB was significantly higher in groups I/R, PF(25) and PF(100) than in group C (P<0.01). And the TNF-alpha level in the supernatants was elevated in groups I/R, PF(25) and PF(100) as compared with that in group C (P<0.01). After pre-treatment with propofol, the mRNA expressions of TLR4 and NF-kappa B and the TNF-alpha level were significantly decreased in groups PF(25) and PF(100) in comparison to those in group I/R (P<0.01). And the decrease in those indicators was more significant in group PF(100) than in group PF(25) (P<0.01). It was concluded that propofol exerted brain-protecting effects during I/R injury by suppressing the mRNA expressions of TLR4 and NF-kappaB and deceasing the TNF-alpha level.
    Journal of Huazhong University of Science and Technology 12/2008; 28(6):711-3. DOI:10.1007/s11596-008-0622-7 · 0.78 Impact Factor
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    ABSTRACT: The cytokine repertoire of ADP/ATP carrier-specific humoral immune responses and the cytokine-dependent anti-ADP/ATP carrier antibody IgG subclasses were examined in a cohort of ADP/ATP carrier-immunized BALB/c mice treated with anti-CD4 monoclonal antibody. Eighteen male BALB/c mice (6-8 weeks old) were randomized into 3 groups: dilated cardiomyopathy (DCM) group, DCM-tolerance (Tol) group and control group. The mice in DCM group were immunized with the peptides derived from human ADP/ATP carrier protein for 6 months and mice in the control group were sham-immunized, while the mice in DCM-Tol group were immunized with ADP/ATP carrier protein and anti-CD4 McAb simultaneously. Serum autoantibody against ADP/ATP carrier and IgG subclasses were measured by ELISA, intracellular cytokines IFN-gamma and IL-4 of Th cells were monitored with flow cytometry, and splenic T cell cytokines IFN-gamma, IL-2, IL-4 and IL-6 were detected by using real-time fluorescent quantitative PCR. The results showed that the autoantibody against ADP/ATP carrier was found in all mice in DCM group, and the antibody level, serum IgG1 and IgG2a subclasses, cytokines in T cells and Th cells were all elevated in DCM group, as compared with those in control group (P<0.01). On the other hand, in DCM-Tol group, the autoantibody level and contents of all the cytokines were significantly different from those in DCM group (P<0.01), and were close to those in control group. And the levels of IgG1, IgG2a, IgG2b and IgG3 were influenced, to varying degrees, by anti-CD4 McAb as compared with those in DCM group. All these four types of IgG subclasses were substantially decreased in DCM-Tol group as compared with DCM group. It is concluded that the treatment with anti-CD4 McAb could prevent the activation of T cells, reverse the abnormal secretion of cytokines and the imbalance between Th1/Th2 cell subsets and abnormal production of autoantibody against ADP/ATP carrier, and eventually avoid myocardial injuries.
    Journal of Huazhong University of Science and Technology 08/2008; 28(4):409-14. DOI:10.1007/s11596-008-0408-y · 0.78 Impact Factor
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    Weikang Zhang · Yueping Long · Jinghui Zhang · Chunyou Wang
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    ABSTRACT: In order to investigate the effects of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on the proliferation, apoptosis of pancreatic cancer cell line SW1990 cells and the expression of cyclin E mRNA, the SW1990 cells were treated with different concentrations of EPA or DHA (20, 40, 60 microg/mL) for 0, 12, 24, 36 and 48 h respectively. By using MTT method, the inhibitory effects of EPA or DHA on the cell growth were assayed. Real time PCR was used to detect the expression changes of cyclin E mRNA after the SW1990 cells were treated with 40 microg/mL EPA or DHA for different time. Flow cytometry was used to test the changes of apoptostic rate in the SW1990 cells treated with different concentrations of EPA or DHA for 24 h. The results showed that EPA and DHA could inhibit the growth of SW1990 cells in a time-and concentration-dependent manner (P<0.01). EPA or DHA could also significantly inhibit the expression of cyclin E mRNA in a time-dependent manner (P<0.05). EPA or DHA could induce the apoptosis of SW1990 cells in a concentration-dependent manner (P<0.01). It was concluded that omega-3 fatty acid could inhibit the proliferation of pancreatic cancer cell line SW1990 cells and promote their apoptosis. The down-regulation of the cyclin E expression by omega-3 fatty acid might be one of the mechanisms for its anti-tumor effect on pancreatic cancer.
    Journal of Huazhong University of Science and Technology 10/2007; 27(5):547-50. DOI:10.1007/s11596-007-0518-y · 0.78 Impact Factor