Jianning Zhang

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

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Publications (57)132.72 Total impact

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    ABSTRACT: miR-221/222 are two highly homologous microRNAs that are frequently upregulated in solid tumors. However, the effects of miR-221/222 in malignant gliomas have not been investigated thoroughly. In this study, we found that miR-221/222 were significantly upregulated in human glioma samples and glioma cell lines. Both gain- and loss-of-function studies showed that miR-221/222 regulate cell proliferation, the cell cycle and apoptosis, in addition to, invasion, metastasis, and angiogenesis in glioma cell lines. Subsequent investigations revealed that TIMP2 is a direct target of miR-221/222, and overexpression of TIMP2 reduced the miR-221/222-mediated invasion, metastasis, and angiogenesis of glioma cells. Taken together, our results suggest that the suppression of miR-221/222 may be a feasible approach for inhibiting the malignant behaviors of glioma.
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    ABSTRACT: The Notch pathway is a highly conserved pathway that regulates hippocampal neurogenesis during embryonic development and adulthood. It has become apparent that intracellular epigenetic modification including DNA methylation is deeply involved in fate specification of neural stem cells (NSCs). However, it is still unclear whether the Notch pathway regulates hippocampal neurogenesis by changing the Notch genes' DNA methylation status. Here, we present the evidence from DNA methylation profiling of Notch1, Hes1 and Ngn2 promoters during neurogenesis in the dentate gyrus (DG) of postnatal, adult and traumatic brains. We observed the expression of Notch1, Hes1 and Ngn2 in hippocampal DG with qPCR, western blot and immunofluorescence staining. In addition, we investigated the methylation status of Notch pathway genes using the bisulfite sequencing PCR (BSP) method. The number of Notch1 or Hes1 (+) and BrdU (+) cells decreased in the subgranular zone (SGZ) of the DG in the hippocampus following TBI. Nevertheless, the number of Ngn2-positive cells in the DG of injured mice was markedly higher than in the DG of non-TBI mice. Accordingly, the DNA methylation level of the three gene promoters changed with their expression in the DG. These findings suggest that the strict spatio-temporal expression of Notch effector genes plays an important role during hippocampal neurogenesis and suggests the possibility that Notch1, Hes1 and Ngn2 were regulated by changing some specific CpG sites of their promoters to further orchestrate neurogenesis in vivo. Copyright © 2015. Published by Elsevier Inc.
    Brain Research Bulletin 02/2015; DOI:10.1016/j.brainresbull.2015.02.003 · 2.97 Impact Factor
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    ABSTRACT: Traumatic brain injury (TBI) is associated with coagulopathy, although it often lacks two key risk factors: severe bleeding and significant fluid resuscitation associated with hemorrhagic shock. The pathogenesis of TBI-associated coagulopathy remains poorly understood. We tested the hypothesis that brain-derived microparticles (BDMPs) released from an injured brain induce a hypercoagulable state that rapidly turns into consumptive coagulopathy. Here, we report that mice subjected to fluid percussion injury (1.9±0.1 atm) developed a BDMP-dependent hypercoagulable state, with peak levels of plasma glial cell and neuronal BDMPs reaching 17,496 ± 4,833/µl and 18,388 ± 3,657/µl, respectively, 3 hrs post TBI. Uninjured mice injected with BDMPs developed a dose-dependent hyper-turned hypo-coagulable state measured by a progressively prolonged clotting time, fibrinogen depletion, and microvascular fibrin deposition in multiple organs. The BDMPs were measured 50 - 300 nm with intact membranes, expressing neuronal or glial cell markers and procoagulant phosphatidylserine and tissue factor. Their procoagulant activity was greater than platelet microparticles and was dose-dependently blocked by lactadherin. Microparticles were produced from injured hippocampal cells, transmigrated through the disrupted endothelial barrier in a platelet-dependent manner, and activated platelets. These data define a novel mechanism of TBI-associated coagulopathy in mice, identify early predictive markers and provide alternative therapeutic targets. Copyright © 2015 American Society of Hematology.
    Blood 01/2015; DOI:10.1182/blood-2014-09-598805 · 9.78 Impact Factor
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    ABSTRACT: Our recent studies have identified increased expression of miR-21 in brain following traumatic brain injury (TBI), which alleviated brain edema that related to the blood-brain barrier (BBB) leakage. To analyze the potential effect of miR-21 on secondary BBB damage after TBI, we employed the fluid percussion injury rat model and manipulated the expression level of miR-21 in brain. We found that miR-21 level in brain microvascular endothelial cells (BMVECs) in lesioned cerebral cortex can be upregulated or downregulated by intracerebroventricular infusion of miR-21 agomir or antagomir. Upregulated miR-21 level conferred a better neurological outcome of TBI, and alleviated TBI-induced secondary BBB damage and loss of tight junction proteins. To explore the molecular mechanism underlying this protective effect, we detected the impact of miR-21 on the expression of Angiopoietin-1(Ang-1) and Tie-2, which can promote the expression of tight junction proteins and amplify BBB stabilization. We found that miR-21 exerts the protective effect on BBB by activating the Ang-1/Tie-2 axis in BMVECs. Thus, miR-21 could be a potential therapeutic target for interventions of secondary BBB damage after TBI. Copyright © 2015. Published by Elsevier B.V.
    Brain Research 01/2015; DOI:10.1016/j.brainres.2015.01.009 · 2.83 Impact Factor
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    ABSTRACT: The aim of the present case study was to investigate the advantages of intraoperative magnetic resonance imaging (iMRI) on the real-time guidance and monitoring of a stereotactic biopsy. The study describes a patient with intracranial lesions, which were examined by conventional MRI and diffusion tensor imaging using a 1.5T intraoperative MRI system. The digital and pre-operative positron emission/computed tomography image data were transferred to a BrainLAB planning workstation, and a variety of images were automatically fused. The BrainLAB software was then used to reconstruct the corticospinal tract (CST) and create a three-dimensional display of the anatomical association between the CST and the brain lesions. A Leksell surgical planning workstation was used to identify the ideal target site and a reasonable needle track for the biopsy. The 1.5T iMRI was used to effectively monitor the intracranial condition during the brain biopsy procedure. Post-operatively, the original symptoms of the patient were not aggravated and no further neurological deficits were apparent. The histopathological diagnosis of non-Hodgkin's B-cell lymphoma was made. Using high-field iMRI, the multi-image fusion-guided stereotactic brain biopsy allows for a higher positive rate of biopsy and a lower incidence of complications. The approach of combining multi-image fusion images with the frame-based stereotactic biopsy may be clinically useful for intracranial lesions of deep functional areas.
    Oncology letters 01/2015; 9(1):223-226. DOI:10.3892/ol.2014.2680 · 0.99 Impact Factor
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    ABSTRACT: To explore the diagnostic and therapeutic values of stereotactic guidance of intraoperative high-field magnetic resonance imaging (iMRI) for multiple intracranial lesions. We retrospectively assessed 18 patients with multiple intracranial lesions undergoing stereotactic guidance of high-field iMRI between June 2011 and May 2013. The procedures included biopsy of stereotactic guidance (n = 6), stereotactic aspiration and drainage for brain abscess (n = 4), stereotactic aspiration and intracavitary irradiation with (32)P for mixed solid and cystic craniopharyngiomas (n = 3) and stereotactic hematoma evacuation (n = 5). For 6 cases with high-field iMRI stereotactic guidance, the target lesions were precisely predetermined and pathological specimens confirmed by clinical follow-up results. For 12 cases with multiple cystic lesions and multiple intracranial hematoma, aspiration of hematoma and liquids was satisfactory. And the course of clinical treatment was significantly shortened. And there was a lower incidence of postoperative complications. iMRI may guide precisely stereotactic surgery. And it has important clinical significance for confirming the diagnosis of multiple intracranial lesions and shortening their treatment courses.
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    ABSTRACT: Cerebral aneurysm (CA) rupture is a major cause of subarachnoid hemorrhage with high morbidity and mortality. Using an animal model, we examined the potential of endothelial colony-forming cells (ECFCs) transfusion on vascular degeneration after CA induction and underlying mechanisms. CA was induced in the right anterior cerebral artery-olfactory artery (ACA/OA) bifurcations in Sprague-Dawley rats with or without ECFCs transfusion. The degeneration of internal elastic lamina (IEL), media thickness and CA size were evaluated. Expression of matrix metalloproteinase-2 and 9 (MMP-2 and 9), tissue inhibitor of metalloproteinase-1 (TIMP-1), macrophage chemoattractant protein-1 (MCP-1), vascular cell adhesion molecule-1 (VCAM-1), nuclear factor κB (NF-κB), endothelial nitric oxide synthase (eNOS), B-cell leukemia/lymphoma-2 (Bcl-2), and inducible nitric oxide synthase (iNOS) were analyzed by quantitative real-time polymerase chain reaction. The macrophages infiltration and apoptosis of smooth muscle cells (SMCs) were examined immunohistologically. Rats in CA+ECFCs transfusion group showed a notable reduction in IEL degeneration, media thinning and CA size compared with those in CA+saline group. ECFCs transfusion inhibited the MMP-driven wall destruction by downregulating MMP-2, MMP-9 expression and upregulating TIMP-1. ECFCs transfusion dramatically decreased VCAM-1 and NF-κB expression, increased eNOS expression and caused no change in MCP-1 expression, which was accompanied by reduced macrophages infiltration. Moreover, ECFCs transfusion reversed downregulation of Bcl-2 expression and upregulation of iNOS expression, and decreased SMCs apoptosis. Collectively, these findings suggest that ECFCs transfusion confers protection against degeneration of aneurysmal wall by inhibiting inflammatory cascades and SMCs apoptosis.
    Brain Research 10/2014; DOI:10.1016/j.brainres.2014.09.077 · 2.83 Impact Factor
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    ABSTRACT: Traumatic brain injury (TBI) is a major cause of chronic disability and death in young adults worldwide. Multiple cellular, molecular and biochemical changes impact the development and outcome of TBI. Neuronal cell apoptosis, which is an important pathological change in secondary brain damage, is crucial to determine the functional recovery after TBI. miR-21, a widely-reported oncogene, which can reduce cell apoptosis in cancer, has been confirmed to be an pronounced up-regulated miRNA after TBI in animal model. Our study is designed to investigate whether miR-21 has the function of antiapoptosis in experimental TBI model in vitro and to explore the possible regulatory mechanism of miR-21 on neuronal apoptosis. The scratch cell injury was performed to mimic TBI-induced apoptosis in neurons, and miR-21 agomir/antagomir was transfected to up-/down-regulate the miR-21 level. Our data suggests that miR-21 can reduce the number of TUNEL-positive neurons. Meanwhile, miR-21 decreased the expression level of PTEN, and increased the phosphorylation of Akt significantly. In neurons transfected with miR-21 agomir, the expression of Bcl-2 was promoted while the caspase-3, caspase-9 and bax level were down-regulated, which are crucially the downstream apoptosis-related proteins of PTEN-Akt signaling pathway. In conclusion, miR-21 can exert the function of reducing neuronal apoptosis through activating the PTEN-Akt signaling pathway. Our research provides new insights into the molecular mechanisms of neuronal apoptosis following TBI, which reminds that miR-21may be a potential therapeutic target for TBI treatment.
    Brain Research 09/2014; 1582. DOI:10.1016/j.brainres.2014.07.045 · 2.83 Impact Factor
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    ABSTRACT: Circulating platelets are anucleated and multi-functional cells that participate in hemostasis and arterial thrombosis. Multiple ligands and mechanical forces activate platelets, leading to cytoskeletal rearrangement and dramatic shape-changes. Such dramatic changes in platelets membrane structures are commonly detected by optical and electron microscopy after platelets are fixed. We have recently developed a method to study the membrane morphology of live platelets using Hopping Probe Ion Conductance Microscopy (HPICM). We have successfully used this technology to study the process of platelet microvesiculation upon exposure to selective agonists. Here, we further discussed technical details of using HPICM to study platelet biology and compared results from HPICM to those from conventional atomic force microscopy and scanning electron microscopy. This method offers several advantages over current technologies. First, it monitors morphological changes of platelets in response to agonists in real time. Second, platelets can be repeatedly scanned over time without damages brought by heat and prolong light exposure. Third, there is no direct contact with platelet surface so that there will no or minimal mechanical damages brought by a cantilever of a conventional atomic force microscopy. Finally, it offers the potential to study platelet membrane ion channels, which have been technically challenging up-to-date. Our data show that HPICM has high-resolution in delineating changes of platelet morphology in response to stimulations and could help to unravel the complex role of platelet in thrombus formation.
    Platelets 08/2014; DOI:10.3109/09537104.2014.940888 · 2.63 Impact Factor
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    ABSTRACT: Previous studies show that circulating endothelial progenitor cells (EPCs) promote angiogenesis, which is a process associated with improved recovery in animal models of traumatic brain injury (TBI), and that recombinant human erythropoietin (rhEPO) plays a protective role following stroke. Thus, it was hypothesized that rhEPO would enhance recovery following brain injury in a rat model of TBI via an increase in the mobilization of EPCs and, subsequently, in angiogenesis. Flow cytometry assays using CD34- and CD133-specific antibodies were utilized to identify alterations in EPC levels, CD31 and CD34 antibody-stained brain tissue sections were used to quantify angiogenesis, and the Morris water maze (MWM) test and the modified Neurological Severity Score (mNSS) test were used to evaluate behavioral recovery. Compared with saline treatment, treatment with rhEPO significantly increased the number of circulating EPCs on days 1, 4, 7, and 14 (P < 0.05), improved spatial learning ability on days 24 and 25 (P < 0.05), and enhanced memory recovery on day 26 (P < 0.05). Moreover, rhEPO treatment decreased mNSS assessment scores on days 14, 21, and 25 (P < 0.05). There was a strong correlation between levels of circulating EPCs and CD34- and CD31-positive cells within the injured boundary zone (CD34(+) r = 0.910, P < 0.01; CD31(+) r = 0.894, P < 0.01) and the ipsilateral hippocampus (CD34(+) r = 0.841, P < 0.01; CD31(+) r = 0.835, P < 0.01). The present data demonstrate that rhEPO treatment improved functional outcomes in rats following TBI via an increase in the mobilization of EPCs and in subsequent angiogenesis.
    Translational Stroke Research 08/2014; 6(1). DOI:10.1007/s12975-014-0362-x
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    ABSTRACT: Hairy and enhancer of split 1 (Hes1), a downstream target of Notch signaling, has long been recognized as crucial in inhibiting neuronal differentiation. However, the role of Hes1 following traumatic brain injury (TBI) in adult neurogenesis in the mouse dentate gyrus (DG) remains partially understood. Here, we investigate the role of Hes1 in regulating neurogenesis in the DG of the adult hippocampus after TBI by up- or down-regulating Hes1 expression. First, adenovirus-mediated gene transfection was employed to up-regulate Hes1 in vivo. The mice were then subjected to TBI, and the hippocampal tissue was collected for western blot analysis at designated times, pre- and post-injury. Moreover, the brain slices were stained for BrdU and doublecortin (DCX). We show that enhancing Hes1 inhibits the proliferation and differentiation of neural precursor cells (NPCs) in the DG of the hippocampus soon after TBI. Second, down-regulation of Hes1 via RNA interference (RNAi) results in a significant increase in neuronal production and promotes the differentiation of NPCs into mature neurons in the DG, as assessed by BrdU and NeuN double staining. Furthermore, a Morris water maze (MWM) test clearly confirmed that the knockdown of Hes1 improves the spatial learning and memory capacity of adult mice following injury. Taken together, these observations suggest that Hes1 represents a negative regulator of adult neurogenesis post-TBI and that the precise space-time regulation of Hes1 expression in the DG may promote the recovery of neural function following TBI.
    Brain Research 07/2014; 1583. DOI:10.1016/j.brainres.2014.07.037 · 2.83 Impact Factor
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    ABSTRACT: The extracellular matrix metalloproteinase inducer (EMMPRIN), or CD147, has been known to play a key regulatory role in vascular permeability and leukocyte activation by inducing the expression of matrix metalloproteinases (MMPs). The effects of traumatic brain injury on the expression of EMMPRIN remain poorly understood. In this study, we investigated changes in EMMPRIN expression in a rat model of fluid percussion injury (FPI) and examined the potential association between EMMPRIN and MMP-9 expression. Adult male rats were subjected to FPI. EMMPRIN expression was markedly up-regulated in the brain tissue surrounding the injured region 6-48h after TBI, as measured by immunoblot and immunohistochemistry. EMMPRIN expression was localized to inflammatory cells. The increase in EMMPRIN expression was temporally correlated with an increase in MMP-9 levels. These data demonstrate, for the first time, changes in CD147 and MMP-9 expression following TBI. These data also suggest that CD147 and MMP-9 may play a role in vascular injuries after TBI.
    Brain Research 06/2014; 1585. DOI:10.1016/j.brainres.2014.06.018 · 2.83 Impact Factor
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    ABSTRACT: Background and purpose It is well known that inflammation influence chronic subdural hematoma (CSDH) formation to a large extent. Atorvastatin has pleiotropic effects on restraining inflammation and promoting angiogenesis besides its cholesterol-lowering function. Hence, atorvastatin may induce anti-inflammation effects and facilitate therapeutic effects for subdural hematoma (SDH). Methods Adult male Wistar rats were subjected to SDH and successful establishment of SDH was confirmed by magnetic resonance imaging (MRI). The treatment was initiated 6 hours after SDH induction. For the treatment, rats suffering SDH were randomly divided into saline group (the control group, rats were treated by saline, n = 29) and atorvastatin group (rats were treated by atorvastatin, 3 mg/kg/day, n = 30). The volume of lesion before treatment as well as on day 2 and day 7 after initial treatment was measured by MRI, respectively. The behaviors before SDH induction and on the days 1, 3, 5 and 7 after the initial treatment were dynamically evaluated. Gene expression, cytokine secretion and the number of neutrophilic granulocyte and vascular density were measured in both neomembrane and SDH lesion on the day 2 and day 7 after the initial treatment. Results It was found that the SDH rats treated by atorvastatin had a better behavior recovery compared to the ones treated by saline (p < 0.05). By virtue of MRI scanning, it was revealed that SDH volumes were eliminated at a high speed by administration of atorvastatin than that of saline. With the help of the microscopic examination in the neomembrane, it was detected that the density of CD31 + neovasculars in the atorvastatin group was significantly higher than that in the saline group and the number of neutrophilic granulocyte in the atorvastatin group is less than that in the saline group. In comparison with saline treatment, the atorvastatin treatment did not change IL-10 expression and secretion, but it significantly decreased TNF-α and IL-6 level as well as VEGF gene expression. Conclusions Atorvastatin treatment may eliminate SDH and improve the neural function of the rats through its anti-inflammatory effects. Hence, it indicated that statin induced inflammatory modulation might play a significant role in rats’ SDH elimination and the functional recovery.
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    ABSTRACT: Objective To investigate the effect of RING finger protein 2 (RNF2) knockdown on the biological characteristics and radiosensitivity in glioma U87 cells. Methods Plasmids containing shRNA targeting RNF2 were transfected into U87 cells. Real-time quantitative PCR (qRT-PCR) and Western blotting were respectively applied to detect the mRNA and protein level of RNF2. MTT assay was used to detect cell proliferation. Cell cycle and apoptosis were measured by flow cytometry combined with annexin V-FITC/PI staining in the control and RNF2 knockdown cells. Apoptosis was also detected after X-ray radiation. Results Both shRNAs efficiently inhibited RNF2 expression in U87 cells. Cell proliferation was obviously depressed in RNF2 knockdown cells. The percentage of cells decreased in S phase (shRNA-NC: 27.31±1.35; shRNF2-1: 16.72±2.90; shRNF2-3: 10.35±1.33) and increased in G1 phase (shRNA-NC: 56.13±1.80; shRNF2-1: 76.32±3.11; shRNF2-3: 80.45±2.83). More cell apoptosis was observed in RNF2 knockdown cells. After X ray radiation, the apoptosis rate was significantly raised in RNF2 knockdown cells (shRNA-NC: 20.88±0.64; shRNF2-1: 39.69±0.57; shRNF2-3: 47.82±0.45). Conclusion Knockdown of RNF2 can inhibit cell proliferation, induce cell cycle arrest and promote apoptosis in U87 cells. RNF2 knockdown can obviously increase the sensitivity of U87 cells to X ray radiation.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 05/2014; 30(5):471-5.
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    ABSTRACT: Traumatic brain injury (TBI) causes deleterious critical-illness-related-corticosteroid-insufficiency (CIRCI), leading to high mortality and morbidity. However, the incidence of CIRCI following different TBI severities is not fully defined. This study was designed to investigate mechanistically the effects of injury severity on corticosteroid response and the development of CIRCI in a rat model of experimentally controlled TBI. Adult male Wistar rats were randomly assigned to sham, mild injury, moderate injury or severe injury groups. TBI was induced using a fluid percussion device at magnitudes of 1.2-1.4atm (mild injury), 2.0-2.2atm (moderate injury), and 3.2-3.5atm (severe injury). We first assessed the effects of injury severity on the mortality and CIRCI occurrence using electrical stimulation test to assess corticosteroid response. We also investigated a series of pathological changes in the hypothalamus, especially in the paraventricular nuclei (PVN), among different injury group including: apoptosis detected by a TUNEL assay, blood-brain-barrier (BBB) permeability assessed by brain water content and Evans Blue extravasation into the cerebral parenchyma, and BBB integrity evaluated by CD31 and Claudin-5 expression and transmission electron microscopy. We made the following observations. First, 6.7% of mild-injured, 13.3% of moderate-injured, and 68.8% of severe-injured rats developed CIRCI, with a peak incidence on post-injury day 7. Second, TBI-induced CIRCI is closely correlated with injury severity. As the injury severity rises both the incidence of CIRCI and mortality surge; Third, increased level of injury severity reduces the expression of endothelial tight junction protein, aggravate BBB permeability and exacerbate the ensuing neural apoptosis in the PVN of hypothalamus. These findings indicate that increased severity of TBI aggravate the incidence of CIRCI by causing damage to tight junctions of vascular endothelial cells and increasing neuronal apoptosis in the PVN of hypothalamus.
    Journal of the neurological sciences 04/2014; 342(1-2). DOI:10.1016/j.jns.2014.04.032 · 2.32 Impact Factor
  • Liang Xue, Shuyuan Yue, Jianning Zhang
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    ABSTRACT: The present study aimed to examine the clinical characteristics of forkhead box protein P1 (FoxP1) in gliomas and its role in the proliferation, invasiveness, migration and apoptosis of the human glioma U251 cell line. The expression levels of FOXP1 were first studied in operation resection specimens of glioma and normal peripheral brain tissues. The enhanced green fluorescent protein (EGFP) expression vector of FOXP1 was prepared and transfected into U251 cells. MTT, cell invasion, transwell and scratch assays were utilized to investigate the cell growth activity and the rate of apoptosis of the cells was tested by flow cytometry. Western blot analysis and quantitative polymerase chain reaction assays were employed to measure the transfection efficacy. The results revealed that FOXP1 was highly expressed in glioma, as compared with low levels detected in normal brain tissues. Following transfection with pEGFP-N1-FOXP1, the proliferation, invasiveness and migration capabilities of cells significantly decreased, whilst the rate of apoptosis was markedly enhanced (P<0.01). Furthermore, the expression of FOXP1 in U251 cells was enhanced (P<0.01). In conclusion, the present study indicated that FOXP1 is closely associated with tumorigenesis and development of glioma, as demonstrated by a reduction in the proliferation, migration and invasion of glioma cells upon FOCP1 overexpression.
    Molecular Medicine Reports 04/2014; 10(1). DOI:10.3892/mmr.2014.2197 · 1.48 Impact Factor
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    ABSTRACT: It is well known that inflammation influence chronic subdural hematoma (CSDH) formation to a large extent. Atorvastatin has pleiotropic effects on restraining inflammation and promoting angiogenesis besides its cholesterol-lowering function. Hence, atorvastatin may induce anti-inflammation effects and facilitate therapeutic effects for subdural hematoma (SDH). Adult male Wistar rats were subjected to SDH and successful establishment of SDH was confirmed by magnetic resonance imaging (MRI). The treatment was initiated 6hours after SDH induction. For the treatment, rats suffering SDH were randomly divided into saline group (the control group, rats were treated by saline, n=29) and atorvastatin group (rats were treated by atorvastatin, 3mg/kg/day, n=30). The volume of lesion before treatment as well as on day 2 and day 7 after initial treatment was measured by MRI, respectively. The behaviors before SDH induction and on the days 1, 3, 5 and 7 after the initial treatment were dynamically evaluated. Gene expression, cytokine secretion and the number of neutrophilic granulocyte and vascular density were measured in both neomembrane and SDH lesion on the day 2 and day 7 after the initial treatment. It was found that the SDH rats treated by atorvastatin had a better behavior recovery compared to the ones treated by saline (p<0.05). By virtue of MRI scanning, it was revealed that SDH volumes were eliminated at a high speed by administration of atorvastatin than that of saline. With the help of the microscopic examination in the neomembrane, it was detected that the density of CD31+ neovasculars in the atorvastatin group was significantly higher than that in the saline group and the number of neutrophilic granulocyte in the atorvastatin group is less than that in the saline group. In comparison with saline treatment, the atorvastatin treatment did not change IL-10 expression and secretion, but it significantly decreased TNF-α and IL-6 level as well as VEGF gene expression. Atorvastatin treatment may eliminate SDH and improve the neural function of the rats through its anti-inflammatory effects. Hence, it indicated that statin induced inflammatory modulation might play a significant role in rats' SDH elimination and the functional recovery.
    Journal of the neurological sciences 04/2014; 341(1-2). DOI:10.1016/j.jns.2014.04.009 · 2.32 Impact Factor
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    ABSTRACT: Involvement of phosphoinositide 3-kinases (PI3Ks) in early aldosterone action on epithelial sodium channel (ENaC) in mammalian renal epithelia was investigated by hopping probe ion conductance microscopy combined with patch-clamping in this study. Aldosterone treatment enlarged the cell volume and elevated the apical membrane of renal mpkCCDc14 epithelia, which resulted in enhancing the open probability of ENaC. Inhibition of PI3K pathway by LY294002 obviously suppressed these aldosterone-induced changes in both cell morphology and ENaC activity. These results indicated the important role of PI3K pathway in early aldosterone action and the close relationship between cell morphology and ENaC activity in mammalian renal epithelia.
    Journal of Membrane Biology 04/2014; DOI:10.1007/s00232-014-9647-y · 2.48 Impact Factor
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    ABSTRACT: Objective To investigate the impact of microRNA-93 on the biological behaviors of A172 glioma cells by observing the changes of cell proliferation, cell cycle and apoptosis. Methods Real-time quantitative PCR (qRT-PCR) was applied to detect the expression of microRNA-93 in 2 samples of human normal brain tissues, 10 samples of glioma tissues and 5 glioma cell lines. Artificially synthesized microRNA-93 mimic was transiently transfected into A172 glioma cells, and then the expression of microRNA-93 was tested by qRT-PCR. MTT assay was used to detect the cell proliferation of A172 glioma cells; apoptosis and cell cycle of A172 glioma cells were measured by flow cytometry. Results MicroRNA-93 was over-expressed in glioma tissues and glioma cell lines as compared with normal samples. The transient transfection of microRNA-93 mimic into A172 glioma cells significantly increased the expression of microRNA-93 in A172 glioma cells, promoted cell proliferation, raised the cell proportion in S phase, reduced the cell proportion in G1 phase, and inhibited cell apoptosis. Conclusion MicroRNA-93 was aberrantly over-expressed in glioma tissues and cell lines. Transient transfection of microRNA-93 mimic led to increased proliferation, G1-to-S cell cycle progression and reduced apoptosis in A172 glioma cells, indicating that micro-RNA-93 might be a new target for the diagnosis and treatment of glioma.
    Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology 04/2014; 30(4):342-5.
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    ABSTRACT: Background: Our study was designed to detect the differentially expressed genes in the injured cerebral cortices compared with normal ones, and to explore a possible new gene target for the treatment of traumatic brain injury. Methods: We used human genome oligonucleotide microarray, which contained 21,329 genes, and compared the gene expression data between 5 cases of traumatic cerebral cortices and 1 normal case of cortices. We randomly selected 2 differentially expressed genes and further confirmed their expression patterns by quantitative polymerase chain reaction (qPCR). Three differentially expressed genes were selected for RT-PCR from 29 cases of contused cerebral cortices. Results: A total of 87 differentially expressed genes were commonly found in all 5 cases of traumatic cerebral tissue, of which 60 were upregulated and 27 were downregulated. Of the upregulated genes, 16 genes were expressed sequence tags or function-unknown fragments, whereas the remaining 44 genes belonged to 12 functional categories. Of the downregulated genes, 20 genes were expressed sequence tags or function-unknown fragments, whereas the remaining 7 genes belonged to 4 functional categories. The results of the gene chips were confirmed by qPCR. The RT-PCR assay showed 3 differentially expressed genes, namely, phosphoprotein 1 (SPP1); cysteine-rich angiogenic inducer 61, (CYR61); and phospholipid scramblase 1 (PLSCR1), the expression level of which were significantly higher than those of the normal ones in the posttraumatic injured cortex. Conclusions: The differentially expressed genes in human injured cerebral cortex screened by gene chips have not been reported, and the intervention with such genes is expected to provide a new gene therapy target for traumatic brain injury.
    Neurosurgery Quarterly 01/2014; 25(1):1. DOI:10.1097/WNQ.0b013e3182a2fe58 · 0.09 Impact Factor