Junwei Hao

Tianjin Medical University, T’ien-ching-shih, Tianjin Shi, China

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Publications (27)127.81 Total impact

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    ABSTRACT: Aims: Long noncoding RNAs (lncRNAs) play a key role in regulating immunological functions. Their impact on the chronic inflammatory disease multiple sclerosis (MS), however, remains unknown. We investigated the expression of lncRNAs in peripheral blood mononuclear cells (PBMCs) of patients with MS and attempt to explain their possible role in the process of MS. Methods: For this study, we recruited 26 patients with MS according to the revised McDonald criteria. Then, we randomly chose 6 patients for microarray analysis. Microarray assays identified outstanding differences in lncRNA expression, which were verified through real-time PCR. LncRNA functions were annotated for target genes using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses, and regulatory relationships between lncRNAs and target genes were analyzed using the "cis" and "trans" model. Results: There were 2353 upregulated lncRNAs, 389 downregulated lncRNAs, 1037 upregulated mRNAs, and 279 downregulated mRNAs in patients with MS compared to healthy control subjects (fold change >2.0). Real-time PCR results of six aberrant lncRNAs were consistent with the microarray data. The coexpression network comprised 864 lncRNAs and 628 mRNAs. Among differentially expressed lncRNAs, 10 lncRNAs were predicted to have 10 cis-regulated target genes, and 33 lncRNAs might regulate their trans target genes. Conclusions: We identified a subset of dysregulated lncRNAs and mRNAs. The differentially expressed lncRNAs may be important in the process of MS. However, the specific molecular mechanisms and biological functions of these lncRNAs in the pathogenesis of MS need further study.
    No preview · Article · Feb 2016 · CNS Neuroscience & Therapeutics
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    ABSTRACT: Myeloid cells, including proinflammatory monocytes and neutrophils, have important roles in the pathology of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). These cells infiltrate the CNS in the early stages of disease development and contribute to the inflammatory response that is associated with symptom severity. It is thus crucial to identify and understand new mechanisms that can regulate the CNS infiltration of proinflammatory myeloid cells. Nicotinic acetylcholine receptors (nAChRs) have been increasingly studied for their immune-regulatory properties. In this study, we assessed the ability of nicotine, an nAChR ligand, to modulate proinflammatory myeloid cell numbers within the bone marrow, spleen, blood, and CNS of EAE mice. We found that nicotine significantly inhibits the infiltration of proinflammatory monocytes and neutrophils into the CNS at time points where these cells are known to play critical roles in disease pathology. In contrast, nicotine does not affect the expansion of other monocytes. We also show that nicotine exerts these effects by acting on α7 and α9 nAChR subtypes. Finally, mRNA transcript levels for CCL2 and CXCL2, chemokines involved in the chemotaxis of proinflammatory monocytes and neutrophils, respectively, are reduced in the brain of nicotine-treated EAE mice before the massive infiltration of these cells. Taken together, our data provide evidence that nAChRs can regulate proinflammatory cell infiltration into the CNS, which could be of significant value for the treatment of neuroinflammatory disorders.
    Full-text · Article · Jan 2016 · The Journal of Immunology
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    ABSTRACT: Post-stroke depression (PSD) and post-stroke fatigue (PSF) are frequent and persistent problems among stroke survivors. Therefore, awareness of signs and symptoms of PSD and PSF is important for their treatment and recovery from stroke. Additionally, since sudden serious illness can result in disequilibrium, early institution of a coping process is essential to restoring stability. The brain damage of stroke leaves patients with unique physical and mental dysfunctions for which coping maybe a key resource while rebuilding lives. We evaluated 368 consecutive patients with acute ischemic stroke for post-stroke emotional disorders at admission and 3 months later. PSD was evaluated by using the Beck Depression Inventory, and PSF was scored with the Fatigue Severity Scale. The Social Support Rating Scale and Medical Coping Modes Questionnaire were also used as measurement tools. Locations of lesions were based on MRI. Those scans revealed infarcts located in the basal ganglia, corona radiate and internal capsule and constituted the independent factors associated with PSF 3 months after stroke occurrence. Conversely, PSD was not related to lesion location. Acceptance-resignation related to PSD and PSF both at admission and 3 months after stroke. Avoidance was the independent factor most closely related to PSD, whereas confrontation was the independent factor best related to PSF at 3 months after stroke onset.
    No preview · Article · Nov 2015 · Journal of Neurology
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    ABSTRACT: Arctigenin is a herb compound extract from Arctium lappa and is reported to exhibit pharmacological properties, including neuronal protection and antidiabetic, antitumor, and antioxidant properties. However, the effects of arctigenin on autoimmune inflammatory diseases of the CNS, multiple sclerosis (MS), and its animal model experimental autoimmune encephalomyelitis (EAE) are still unclear. In this study, we demonstrated that arctigenin-treated mice are resistant to EAE; the clinical scores of arctigenin-treated mice are significantly reduced. Histochemical assays of spinal cord sections also showed that arctigenin reduces inflammation and demyelination in mice with EAE. Furthermore, the Th1 and Th17 cells in peripheral immune organs are inhibited by arctigenin in vivo. In addition, the Th1 cytokine IFN-γ and transcription factor T-bet, as well as the Th17 cytokines IL-17A, IL-17F, and transcription factor ROR-γt are significantly suppressed upon arctigenin treatment in vitro and in vivo. Interestedly, Th17 cells are obviously inhibited in CNS of mice with EAE, while Th1 cells do not significantly change. Besides, arctigenin significantly restrains the differentiation of Th17 cells. We further demonstrate that arctigenin activates AMPK and inhibits phosphorylated p38, in addition, upregulates PPAR-γ, and finally suppresses ROR-γt. These findings suggest that arctigenin may have anti-inflammatory and immunosuppressive properties via inhibiting Th17 cells, indicating that it could be a potential therapeutic drug for multiple sclerosis or other autoimmune inflammatory diseases.
    No preview · Article · Oct 2015 · Molecular Neurobiology
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    ABSTRACT: Vascular dementia (VaD) is a progressive and highly prevalent disorder. However, in a very large majority of cases, a milieu of cellular and molecular events common for multiple neurodegenerative diseases is involved. Our work focused on whether the immunomodulating effect of glatiramer acetate (GA) could restore normalcy to the microenvironment and ameliorate cognitive decline induced by chronic cerebral hypoperfusion. We assessed cognitive function by rats' performance in a Morris water maze (MWM), electrophysiological recordings and by pathologic changes. The results suggest that GA reduced cognitive deficits by reestablishing an optimal microenvironment such as increasing expression of the brain-derived neurotrophic factor (BDNF) and modulating the Th1/Th2 cytokine balance in the hippocampus. When microenvironmental homeostasis is restored, cholinergic activity becomes involved in ameliorating cellular damage. Since vaccination with GA can boost "protective autoimmunity" in this way, a similar strategy may have therapeutic potential for alleviating VaD disease.
    Preview · Article · Sep 2015 · Scientific Reports
  • Yang Yao · Zengguang Wang · Weidong Yang · Junwei Hao

    No preview · Article · Jun 2015 · Annals of Pharmacotherapy
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    ABSTRACT: Post-stroke depression (PSD) and post-stroke emotional incontinence (PSEI) has attracted world-wide interest in recent years. These emotional disturbances have a negative impact on the rehabilitation process and the associated worse outcome. Consequently, defining the risk factors for development of PSD and PSEI is important. In this study, we evaluated 368 consecutive patients with acute ischemic stroke at admission and at 3 months later. PSD was evaluated by using the Beck Depression Inventory (BDI), and PSEI was evaluated using Kim's criteria. The Social Support Rating Scale (SSRS) and Medical Coping Modes Questionnaire (MCMQ) were also used as measurement tools. Multivariate analyses showed that anterior cortex infarction was associated with PSEI 3 months after stroke occurrence. The appearance of PSD was not related to lesion location. Both motor and sensory dysfunction was independently associated with PSD at admission, whereas low degree of social utilization was the independent factor associated with PSD 3 months after stroke. Acceptance-resignation related to PSD and PSEI both at admission and 3 months after stroke. Avoidance was the independent factor related to PSD at 3 months after stroke onset.
    No preview · Article · May 2015 · The International journal of neuroscience
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    ABSTRACT: Peripheral lymphocytes entering brain ischemic regions orchestrate inflammatory responses, catalyze tissue death, and worsen clinical outcomes of acute ischemic stroke (AIS) in preclinical studies. However, it is not known whether modulating brain inflammation can impact the outcome of patients with AIS. In this open-label, evaluator-blinded, parallel-group clinical pilot trial, we recruited 22 patients matched for clinical and MRI characteristics, with anterior cerebral circulation occlusion and onset of stroke that had exceeded 4.5 h, who then received standard management alone (controls) or standard management plus fingolimod (FTY720, Gilenya, Novartis), 0.5 mg per day orally for 3 consecutive days. Compared with the 11 control patients, the 11 fingolimod recipients had lower circulating lymphocyte counts, milder neurological deficits, and better recovery of neurological functions. This difference was most profound in the first week when reduction of National Institutes of Health Stroke Scale was 4 vs. -1, respectively (P = 0.0001). Neurological rehabilitation was faster in the fingolimod-treated group. Enlargement of lesion size was more restrained between baseline and day 7 than in controls (9 vs. 27 mL, P = 0.0494). Furthermore, rT1%, an indicator of microvascular permeability, was lower in the fingolimod-treated group at 7 d (20.5 vs. 11.0; P = 0.005). No drug-related serious events occurred. We conclude that in patients with acute and anterior cerebral circulation occlusion stroke, oral fingolimod within 72 h of disease onset was safe, limited secondary tissue injury from baseline to 7 d, decreased microvascular permeability, attenuated neurological deficits, and promoted recovery.
    Full-text · Article · Dec 2014 · Proceedings of the National Academy of Sciences
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    ABSTRACT: Inflammation and oxidative stress play an important part in the pathogenesis of focal cerebral ischemia/reperfusion (I/R) injury, resulting in neuronal death. The signaling pathways involved and the underlying mechanisms of these events are not fully understood. Chrysin, which is a naturally occurring flavonoid, exhibits various biological activities. In this study, we investigated the neuroprotective properties of chrysin in a mouse model of middle cerebral artery occlusion (MCAO). To this end, male C57/BL6 mice were pretreated with chrysin once a day for seven days and were then subjected to 1 h of middle cerebral artery occlusion followed by reperfusion for 24 h. Our data show that chrysin successfully decreased neurological deficit scores and infarct volumes, compared with the vehicle group. The increases in glial cell numbers and proinflammatory cytokine secretion usually caused by ischemia/reperfusion were significantly ameliorated by chrysin pretreatment. Moreover, chrysin also inhibited the MCAO-induced up-regulation of nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS), compared with the vehicle. These results suggest that chrysin could be a potential prophylactic agent for cerebral ischemia/reperfusion (I/R) injury mediated by its anti-inflammatory and anti-oxidative effects.
    Preview · Article · Nov 2014 · International Journal of Molecular Sciences
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    Chao Zhang · Bingdi Xie · Fu-Dong Shi · Junwei Hao

    Preview · Article · Aug 2014 · Journal of Neurology Neurosurgery & Psychiatry
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    ABSTRACT: Plumbagin (PL, 5-hydroxy-2-methyl-1,4-naphthoquinone) is an herbal compound derived from medicinal plants of the Droseraceae, Plumbaginaceae, Dioncophyllaceae, and Ancistrocladaceae families. Reports have shown that PL exerts immunomodulatory activity and may be a novel drug candidate for immune-related disease therapy. However, its effects on dendritic cells (DCs), the most potent antigen-presenting cells (APCs), remain unclear. In this study, we demonstrate that PL inhibits the differentiation, maturation, and function of human monocyte-derived DCs. PL can also restrict the expression of Th1- and Th17-polarizing cytokines in mDC. In addition, PL suppresses DCs both in vitro and in vivo, as demonstrated by its effects on the mouse DC line DC2.4 and mice with experimental autoimmune encephalomyelitis (EAE), respectively. Notably, PL ameliorated the clinical symptoms of EAE, including central nervous system (CNS) inflammation and demyelination. Our results demonstrate the immune suppressive and anti-inflammatory properties of PL via its effects on DCs and suggest that PL could be a potential treatment for DC-related autoimmune and inflammatory diseases.
    No preview · Article · Aug 2014 · Journal of Neuroimmunology
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    ABSTRACT: Importance Pronounced inflammatory reactions occurring shortly after intracerebral hemorrhage (ICH) contribute to the formation and progression of perihematomal edema (PHE) and secondary brain injury. We hypothesized that modulation of brain inflammation reduces edema, thus improving clinical outcomes in patients with ICH.Objective To investigate whether oral administration of fingolimod, a Food and Drug Administration–approved sphingosine 1–phosphate receptor modulator for multiple sclerosis, is safe and effective in alleviating PHE and neurologic deficits in patients with ICH.Design, Setting, and Participants In this 2-arm, evaluator-blinded study, we included 23 patients with primary supratentorial ICH with hematomal volume of 5 to 30 mL. Clinical and neuroimaging feature–matched patients were treated with standard care with or without oral fingolimod. The study was conducted in Tianjin Medical University General Hospital, Tianjin, China.Interventions All patients received standard management alone (control participants) or combined with fingolimod (FTY720, Gilenya), 0.5 mg, orally for 3 consecutive days. Treatment was initiated within 1 hour after the baseline computed tomographic scan and no later than 72 hours after the onset of symptoms.Main Outcomes and Measures Neurologic status and hematomal and PHE volumes (Ev) and relative PHE, defined as Ev divided by hematomal volume, were monitored by clinical assessment and magnetic resonance imaging, respectively, for 3 months.Results Patients treated with fingolimod exhibited a reduction of neurologic impairment compared with control individuals, regained a Glasgow Coma Scale score of 15 by day 7 (100% vs 50%, P = .01), and had a National Institutes of Health Stroke Scale score reduction of 7.5 vs 0.5 (P < .001). Neurologic functions improved in these patients in the first week coincident with a reduction of circulating lymphocyte counts. At 3 months, a greater proportion of patients receiving fingolimod achieved full recovery of neurologic functions (modified Barthel Index score range, 95-100; 63% vs 0%; P = .001; modified Rankin Scale score range, 0-1; 63% vs 0%; P = .001), and fewer reported ICH-related lung infections. Perihematomal edema volume and rPHE were significantly smaller in fingolimod-treated patients than in control individuals (Ev at day 7, 47 mL vs 108 mL, P = .04; Ev at day 14, 55 mL vs 124 mL, P = .07; rPHE at day 7, 2.5 vs 6.4, P < .001; rPHE at day 14, 2.6 vs 7.7, P = .003, respectively). We recorded no differences between groups in the occurrence of adverse events.Conclusions and Relevance In patients with small- to moderate-sized deep primary supratentorial ICH, administration of oral fingolimod within 72 hours of disease onset was safe, reduced PHE, attenuated neurologic deficits, and promoted recovery. The efficacy of fingolimod in preventing secondary brain injury in patients with ICH warrants further investigation in late-phase trials.Trial Registration clinicaltrials.gov Identifier:NCT02002390
    No preview · Article · Jul 2014 · JAMA Neurology
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    ABSTRACT: Guillain-Barré syndrome (GBS) is an acute, post-infectious, immune-mediated, demyelinating disease of peripheral nerves and nerve roots. Experimental autoimmune neuritis (EAN) is an animal model of GBS. Chrysin, which is a naturally occurring flavonoid, exhibits various biological activities. This study was designed to investigate the anti-inflammatory and neuroprotective properties of preventative and therapeutic chrysin treatment in EAN rats. For preventative treatment, chrysin was administered orally from day 1 to day 16 (50 mg/kg once daily) while, for therapeutic treatment, rats received chrysin from day 7 to day 16 at the same dose once daily. Control animals received the same volume of the vehicle (PBS/2% DMSO). Regardless of the treatment regimen, chrysin attenuated the severity and duration of the clinical course of EAN and reduced inflammatory cell infiltration and demyelination of sciatic nerves. In the sciatic nerves, the expression of inducible nitric oxide synthase, cyclooxygenase-2 and nuclear factor kappa B was reduced. Furthermore, chrysin inhibited the splenic mononuclear cell secretion of IL-1β, IL-2, IL-6, IL-12, IFN-γ and TNF-α, and elevated the level of IL-4. In summary, our data demonstrate that chrysin is a potentially useful agent for the treatment of EAN with its anti-inflammatory and neuroprotective effect.
    Full-text · Article · Jan 2014 · Neuroscience
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    ABSTRACT: Glatiramer acetate (GA) is one of the first-line disease-modifying medications that have been approved for the treatment of multiple sclerosis via immune modulatory mechanisms. However, it remains unclear whether the immunomodulation effect of GA is central nervous system (CNS) antigen specific. Here, we explored the mechanism of action of GA by subcutaneously injecting GA in experimental autoimmune neuritis (EAN) rats, an animal model for Guillain-Barré syndrome (GBS). Clinical, electrophysiological and histological findings showed that neurological deficits, demyelination and axonal injury of sciatic nerves were all significantly attenuated in Lewis rats when GA was administered before immunization with peripheral nervous system antigen P0. Our results further demonstrated that GA treatment inhibited either P0 or myelin basic protein (MBP) (CNS antigen)-stimulated auto-immune T-cell proliferation in vitro. GA administrated at 10 days after induction of EAN when neurological sign became apparent also ameliorated the severity of disease, inhibited T-cell response to P0 and MBP and induced shift of proinflammatory and immune modulatory cytokines. Collectively, our findings suggested that GA attenuated neurological deficits in EAN rats and that the immune modulatory mechanisms of GA were not CNS antigen specific.Immunology and Cell Biology advance online publication, 26 November 2013; doi:10.1038/icb.2013.81.
    No preview · Article · Nov 2013 · Immunology and Cell Biology
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    ABSTRACT: Embelin (2,5-dihydroxy-3-undecyl-1,4-benzoquinone, EB) has been shown to inhibit the X-linked inhibitor of apoptosis protein and various inflammatory pathways. Although different molecular mechanisms have been described for the potent antitumor activities of EB, its potential effect on inflammatory and immune-mediated diseases such as multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) remains unclear. In this study, we demonstrated that EB suppressed human CD14(+) monocyte-derived dendritic cell (DC) differentiation, maturation, and endocytosis and further inhibited the stimulatory function of mature DCs on allogeneic T cell proliferation in vitro. In addition, EB blocked the DC-derived expression of the Th1 cell-polarizing cytokines interferon-γ and interleukin (IL)-12 and the Th17 cell-polarizing cytokines IL-6 and IL-23. In vivo administration of EB led to a reduction in the EAE clinical score, in central nervous system inflammation, and in demyelination. Furthermore, EB also suppressed inflammatory Th1 and Th17 cells in EAE, at least partially, through the promotion of transforming growth factor-beta and β-catenin expression and inhibition of signal transducer and activator of transcription 3 signaling pathways in DCs. These data suggest that EB has potent anti-inflammatory and immunosuppressive properties and is a potential therapeutic drug for MS and other autoimmune inflammatory diseases.
    No preview · Article · Nov 2013 · Molecular Neurobiology
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    ABSTRACT: Guillain-Barré syndrome (GBS) is an acute and usually monophasic, neurological, demyelinating disease. Although most patients have good outcomes without sequelae after conventional plasma exchange and intravenous immunoglobulin therapy, 20 % of patients continue to have severe disease and 5 % die of their disease. Therefore, there is an obvious need for more acceptable and efficacious therapies. Experimental autoimmune neuritis (EAN) is the classical animal model for GBS. As there is no specific drug for GBS, several drugs targeting the humoral and cellular components of the immune response have been used to treat EAN in the endeavour to find new treatment alternatives for GBS. This review focused on some new strategies for GBS, which have been reported but have not yet been widely used, and on the main drugs which have been investigated in EAN.
    No preview · Article · Sep 2013 · Clinical Reviews in Allergy & Immunology
  • Yang Yao · Alain R Simard · Fu-Dong Shi · Junwei Hao
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    ABSTRACT: IL-10 is an anti-inflammatory cytokine that plays a significant role in controlling inflammation and modulating adaptive immune responses that cause tissue damage. IL-10-producing lymphocytes contribute to the delicate balance between inflammation and immunoregulation, and are thus regarded as a kind of "regulatory cells." Dysregulation of these cells is linked with susceptibility to numerous inflammatory diseases. In this review, we summarized what is known about the regulatory effects of IL-10 produced by lymphocytes, including T cells, B cells and natural killer cells, in inflammatory diseases. We hope to augment immune responses or prevent immunopathology through making some small changes in the levels of IL-10 produced by lymphocytes, or in the cellular location where it is produced.
    No preview · Article · Apr 2013 · International Reviews Of Immunology
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    ABSTRACT: Cigarette smoke exposure markedly compromises the ability of the immune system to protect against invading pathogens and tumorigenesis. Nicotine is a psychoactive component of tobacco products that acts as does the natural neurotransmitter, acetylcholine, on nicotinic receptors (nAChRs). Here we demonstrate that natural killer (NK) cells strongly express nAChR β2. Nicotine exposure impairs the ability of NK cells to kill target cells and release cytokines, a process that is largely abrogated by nAChR β2 deficiency. Further, nicotinic suppression of NF-κB-induced transcriptional activity in NK cells is dependent on nAChR β2. This nAChR subtype also plays a large role in the NK cell-mediated control of melanoma lung metastasis, in a murine lung metastasis model exposed to nicotine. Our findings suggest nAChR β2 as a prominent pathway for nicotine induced impairment of NK cell functions which contributes to the occurrence of smoking-related pathologies.
    Full-text · Article · Feb 2013 · PLoS ONE
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    ABSTRACT: The matrix-degrading metalloproteinases (MMPs), particularly MMP-9, play important roles in the pathogenesis and development of malignant gliomas. In the present study, the oncogenic role of MMP-9 in malignant glioma cells was investigated via antisense RNA blockade in vitro and in vivo. TJ905 malignant glioma cells were transfected with pcDNA3.0 vector expressing antisense MMP-9 RNA (pcDNA-ASMMP9), which significantly decreased MMP-9 expression, and cell proliferation was assessed. For in vivo studies, U251 cells, a human malignant glioma cell line, were implanted subcutaneously into 4- to 6-week-old BALB/c nude mice. The mice bearing well-established U251 gliomas were treated with intratumoral pcDNA-AS-MMP9-Lipofectamine complex (AS-MMP-9-treated group), subcutaneous injection of endostatin (endostatin-treated group), or both (combined therapy group). Mice treated with pcDNA (empty vector)-Lipofectamine served as the control group. Four or eight weeks later, the volume and weight of tumor, MMP-9 expression, microvessel density and proliferative activity were assayed. We demonstrate that pcDNA-AS-MMP9 significantly decreased MMP-9 expression and inhibited glioma cell proliferation. Volume and weight of tumor, MMP-9 expression, microvessel density and proliferative activity in the antisense-MMP-9-treated and therapeutic alliance groups were significantly lower than those in the control group. The results suggest that MMP-9 not only promotes malignant glioma cell invasiveness, but also affects tumor cell proliferation. Blocking the expression of MMP-9 with antisense RNA substantially suppresses the malignant phenotype of glioma cells, and thus can be used as an effective therapeutic strategy for malignant gliomas.
    No preview · Article · Jan 2013 · Neuroscience Bulletin
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    ABSTRACT: Vorinostat, a histone deacetylase inhibitor, has been used clinically as an anticancer drug and also has immunosuppressive properties. However, the underlying mechanisms of effects of vorinostat on central nervous system (CNS) inflammatory diseases remain incomplete. Here, this study investigates the effects of vorinostat on human CD14(+) monocyte-derived dendritic cells (DCs) and mouse immature DC in vitro. Furthermore, we explore the therapeutic effects and cellular mechanisms of vorinostat on animal model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE) in vivo. Our findings demonstrate that vorinostat inhibited human CD14(+) monocyte-derived DCs differentiation, maturation, endocytosis, and further inhibited mDC's stimulation of allogeneic T-cell proliferation. In addition, vorinostat inhibited DC-directed Th1- (Type 1T helper) and Th17-polarizing cytokine production. Furthermore, vorinostat ameliorated Th1- and Th17-mediated EAE by reducing CNS inflammation and demyelination. What's more, Th1 and Th17 cell functions were suppressed in vorinostat-treated EAE mice. Finally, vorinostat suppressed expression of costimulatory molecules of DC in EAE mice. These suggest therapeutic effects of vorinostat on EAE which may by suppress DCs and DCs-mediated Th1 and Th17 cell functions. Our findings warrant further investigation in the potential of vorinostat for the treatment of human multiple sclerosis.
    No preview · Article · Dec 2012 · Experimental Neurology

Publication Stats

296 Citations
127.81 Total Impact Points

Institutions

  • 2011-2015
    • Tianjin Medical University
      T’ien-ching-shih, Tianjin Shi, China
  • 2009-2012
    • Barrow Neurological Institute
      • Department of Neurology
      Phoenix, Arizona, United States
  • 2010-2011
    • Nankai University
      • School of Medicine
      T’ien-ching-shih, Tianjin Shi, China