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ABSTRACT: As one part of epigenetics, histone deacetylases (HDACs) have been demonstrated to get into the neural events, including neurogenesis, synaptic plasticity, and neurodegeneration through regulating acetylation status of target proteins to influence protein function and gene expression. However, the recent studies indicated that HDAC2, a member of HDACs family, played a role in insulin signaling pathway and synaptic plasticity. Here, we are concerned about whether HDAC2 was co-located with insulin signaling components in postsynaptic glutamatergic neurons (PSGNs) of the adult mouse hippocampus using double immunofluorescence staining. The results displayed that HDAC2 was present in PSGNs marked by N-methyl-D: -aspartate receptor subunit 2B, in which major components of insulin signaling pathway such as insulin receptor alpha and beta and insulin receptor substrate-1 were also involved. Accordingly, we speculate that the interaction of HDAC2 and insulin signaling system in PSGNs observed in the present study may serve as a potential mechanism in memory formation. We hope this could provide a valuable basis for understanding the roles of HDAC2 and insulin on cognitive impairment of diabetes mellitus, involved Alzheimer's disease, which is also called type 3 diabetes recently. And this will also benefit to the treatment of insulin-related diseases in the central nervous system.
Cellular and Molecular Neurobiology 06/2012; · 1.97 Impact Factor
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ABSTRACT: To explore the role of actin-bundling protein, fascin during the progression of pancreatic cancer.
The plasmid expressing human fascin-1 was stably transfected into the pancreatic cancer cell line MIA PaCa-2. The proliferation, cell cycle, motility, scattering, invasiveness and organization of the actin filament system in fascin-transfected MIA PaCa-2 cells and control non-transfected cells were determined.
Heterogeneous overexpression of fascin markedly enhanced the motility, scattering, and invasiveness of MIA PaCa-2 cells. However, overexpression of fascin had minimal effect on MIA PaCa-2 cell proliferation and cell cycle. In addition, cell morphology and organization of the actin filament system were distinctly altered in fascin overexpressed cells. When transplanted into BALB/c-nu mice, fascin-transfected pancreatic cancer cells developed solid tumors at a slightly slower rate, but these tumors displayed more aggressive behavior in comparison with control tumors.
Fascin promotes pancreatic cancer cell migration, invasion and scattering, thus contributes to the aggressive behavior of pancreatic cancer cells.
World Journal of Gastroenterology 10/2011; 17(40):4470-8. · 2.47 Impact Factor
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Jia-Mei Li,
Hua Zhu,
Shan Lu,
Ying Liu,
Qin Li,
Paula Ravenscroft, Yan-Feng Xu,
Lan Huang,
Chun-Mei Ma,
Erwan Bezard,
Robert Chun-Hua Zhao,
Ren-Zhi Wang,
Chuan Qin
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ABSTRACT: Transplanted mesenchymal stem cells migrate toward brain lesions and differentiate into neurons, glial cells, and neural stem cells in diseased or injured animal models. The migratory routes and differentiation patterns of mesenchymal stem cells in normal rats are, however, unknown. Here, labelled human mesenchymal stem cells (or saline) were transplanted into the striatum of adult rats to observe their migration and differentiation.
Labelled human mesenchymal stem cells were transplanted into the right striatum of adults rats (n = 24). Brain sections were examined for migratory routes of labelled human mesenchymal stem cells by immunohistochemistry method, fluorescence microscope and laser scanning confocal microscopy observation, and Prussian blue staining. Moreover, the differentiation of human mesenchymal stem cells was detected by double immunohistochemistry.
After 3 days, most human mesenchymal stem cells resided around the injection sites. Human mesenchymal stem cells were found in or around the corpus callosum and the subependymal layer after 7 days. A great number of human mesenchymal stem cells were detected throughout the brain on both ipsilateral and contralateral sides after 14 days. A high concentration of donor cells persisted in the corpus callosum, the external capsule and the subventricular zone. In addition, the incorporated human mesenchymal stem cells were neuronal nuclei- and glial fibrillary acidic protein-positive.
Human mesenchymal stem cells migrate throughout the brain mainly along with the axis of corpus callosum external capsule and the subependymal layer, and differentiate into neurons and astrocytes rather than neural stem cells.
Neurological Research 01/2011; 33(1):84-92. · 1.52 Impact Factor
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ABSTRACT: For the purpose of investigating the effects of S100B on the development of Parkinsion's disease (PD), a high-performance liquid chromatography coupled with electrospray ionization time-of-flight mass spectrometry (HPLC/MS-ESI-TOF) metabonomic approach was established to study the mesencephalon profiling of brain-specific human S100B transgenic mice. In order to obtain more full-scale chemical information of metabolites, two kinds of separation mechanism, including reversed-phase (RP) column chromatography and hydrophilic interaction liquid chromatography (HILIC) column, were combined to use. Acquired data were subjected to principal component analysis (PCA) to investigate the effects of S100B protein on mice mesencephalon metabolite profiles. Potential biomarkers were screened by using Mass Hunter Prossional Profiller (MPP) and were identified by the accurate mass. Twelve metabolites in mesencephalon of S100B transgenic mice were identified as potential biomarkers, among which, glutamic acid (Glu) detected by RP/MS in negative ionization mode, gamma-aminobutyric acid (GABA) and tryptophan (Trp) detected by HILIC/MS in positive ionization mode, phenylalanine (Phe) and histidine (His) detected by HILIC/MS in negative ionization mode, related to metabolic pathway of neurotransmitters in mice central nervous system. The analytical technique used in this paper was able to detect biochemical changes in mesencephalon of S100B transgenic mice, which may be helpful to understand the action mechanism of S100B protein in the development of PD.
Biological & Pharmaceutical Bulletin 01/2011; 34(6):871-6. · 1.66 Impact Factor
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Jiang Ning Liu,
Wei Wang,
Jian Ying Duo,
Yi Hao,
Chun Mei Ma,
Wan Bo Li,
Shu Zhu Lin,
Xue Zhong Gao,
Xiao Lin Liu, Yan Feng Xu,
Wen-Bo Xu,
Chuan Qin,
Lian Feng Zhang
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ABSTRACT: Human enterovirus 71 (EV71) is a cause of hand, foot and mouth disease (HMFD) in children under 6 years old, and could cause serious neurological complications in some patients. Numerous large outbreaks of EV71 caused HMFD have occurred recently in Asia, especially in China. The cross-reactivity of EV71 with human brain tissue was observed and the cross-reactivity inducing regions were identified in previously study, which suggested that there were two regions in structural proteins of virus should be avoided in the vaccine. Six peptides without cross-reactivity were selected and combined into three vaccine candidates and applied in further evaluation in neonatal mice. The Vac6 comprising the peptides of P(70-159), P(140-249), P(324-443) and P(746-876) of the structural proteins could provide effective protection on pups against virus infection, as shown in viral copies detection and histopathology examination. Immunohistochemical staining results indicated that Vac6 had no cross-reactivity with human brain tissues. Our results suggested that Vac6 could have potential clinical value against EV71 epidemics caused mainly by C4 strains in the mainland of China.
Vaccine 10/2010; 28(46):7444-51. · 3.77 Impact Factor
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Chun Shi Jia,
Jiang Ning Liu,
Wan Bo Li,
Chun Mei Ma,
Shu Zhu Lin,
Yi Hao,
Xue Zhong Gao,
Xiao Lin Liu, Yan Feng Xu,
Lian Feng Zhang,
Chuan Qin
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ABSTRACT: EV71 occasionally cause a series of severe neurological symptoms, including aseptic meningitis, encephalitis, and poliomyelitis-like paralysis. However, the neurological destruction mechanism was remained to be clarified. This study described the cross reaction between EV71 induced IgG and human brain tissue.
Cross reaction of the IgG from 30 EV71 infected patients' sera to human tissues of cerebra was observed, which suggested that some EV71 antigens could induce IgG cross-reactivity to human cerebra. To identify the regions of EV71 virus that containing above antigens, the polypeptide of virus was divided into 19 peptides by expression in prokaryotes cell. Mouse anti-sera of these peptides was prepared and applied in immunohistochemical staining with human adult and fetus brain tissue, respectively. The result indicated the 19 peptides can be classified into three groups: strong cross-reactivity, weak cross-reactivity and no cross-reactivity with human brain tissue according the cross reaction activity. Then, the increased Blood Brain Barrier (BBB) permeability and permits IgG entry in neonatal mice after EV71 infection was determined.
EV71 induced IgG could enter BBB and cross-reacted with brain tissue in EV71 infected neonatal mice, and then the peptides of EV71 that could induce cross-reactivity with brain tissue were identified, which should be avoided in future vaccine designing.
Virology Journal 02/2010; 7:47. · 2.34 Impact Factor
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Zhonghua bing li xue za zhi Chinese journal of pathology 11/2008; 37(10):711-2.
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Xiu-Hong Yang,
Wei Deng,
Zan Tong,
Yan-Xia Liu,
Lian-Feng Zhang,
Hua Zhu,
Hong Gao,
Lan Huang,
Ya-Li Liu,
Chun-Mei Ma, Yan-Feng Xu,
Ming-Xiao Ding,
Hong-Kui Deng,
Chuan Qin
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ABSTRACT: To establish a small animal model of severe acute respiratory syndrome (SARS), we developed a mouse model of human severe acute respiratory syndrome coronavirus (SARS-CoV) infection by introducing the human gene for angiotensin-converting enzyme 2 (hACE2) (the cellular receptor of SARS-CoV), driven by the mouse ACE2 promoter, into the mouse genome. The hACE2 gene was expressed in lung, heart, kidney, and intestine. We also evaluated the responses of wild-type and transgenic mice to SARS-CoV inoculation. At days 3 and 7 postinoculation, SARS-CoV replicated more efficiently in the lungs of transgenic mice than in those of wild-type mice. In addition, transgenic mice had more severe pulmonary lesions, including interstitial hyperemia and hemorrhage, monocytic and lymphocytic infiltration, protein exudation, and alveolar epithelial cell proliferation and desquamation. Other pathologic changes, including vasculitis, degeneration, and necrosis, were found in the extrapulmonary organs of transgenic mice, and viral antigen was found in brain. Therefore, transgenic mice were more susceptible to SARS-CoV than were wild-type mice, and susceptibility was associated with severe pathologic changes that resembled human SARS infection. These mice will be valuable for testing potential vaccine and antiviral drug therapies and for furthering our understanding of SARS pathogenesis.
Comparative medicine 11/2007; 57(5):450-9. · 1.05 Impact Factor
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ABSTRACT: To reconstruct of a tissue engineering skin in vitro for the study of the use of drug percutaneous penetration and metabolism.
Dermal fibroblasts were embedded in collagen type I. HaCaT cells were seeded on the top of the gel. The skin was generated through air-liquid interface culture. Effects of various culture media on tissues morphology were investigated. Sections of the cultured skin were stained with hematoxylin and eosin and examined under microscope. Permeation and metabolism of ketoprofen and its isopropyl ester through the cultured skin were investigated.
HaCaT cells initially developed a multilayer epithelium at the air-liquid interface, but it showed a parakeratotic stratum corneum. Vitamin C enhanced cell proliferation obviously. Vitamin D3 promoted cell differentiation. And estradiol showed little effect on the tissue engineering skin. Ketoprofen isopropyl ester was hydrolyzed into ketoprofen when penetrated through the cultured skin, which resembled in the skin cell homogenates metabolism.
Cultured at the air-liquid interface, HaCaT cells developed a parakeratotic mutilayer epithelium. Enzyme activity was reserved. This cultured skin could serve as an appropriate model for drug percutaneous metabolism and skin irritation.
Yao xue xue bao = Acta pharmaceutica Sinica 10/2005; 40(9):782-6.
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ABSTRACT: To study the intervention of cetirizine on monocyte chemoattractant protein-1 (MCP-1) in different cutaneous inflammation models.
Histamine and IFN-gamma stimulated dermal fibroblast cells and HaCaT cells to mimic cutaneous inflammation. Expression of MCP-1 was assessed by means of RT-PCR and ELISA.
Compared with the control group of dermal fibroblast (DF) cells and HaCaT cells, MCP-1 mRNA was significantly upregulated by histamine (10 micromol x L(-1)) and IFN-gamma (20 ng x mL(-1)). The protein secretions of MCP-1 were increased 3.5 fold and 8.4 fold in DF cells, respectively. The similar tendency was observed in HaCaT cells. The enhancing effects of histamine and IFN-gamma on MCP-1 protein production were significantly inhibited by cetirizine (1 and 10 micromol x L(-1)) in DF and HaCaT cells.
Cetirizine may exert the anti-inflammatory effect of skin via inhibiting MCP-1 expression.
Yao xue xue bao = Acta pharmaceutica Sinica 06/2005; 40(5):414-7.
