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Berlin Brandenburg

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  • 1
    Language: English
    In: Journal of neurochemistry, July 2011, Vol.118(1), pp.93-104
    Description: Human immunodeficiency virus (HIV)-1-associated neurocognitive disorders (HAND) associated with infection and activation of mononuclear phagocytes (MP) in the brain, occur late in disease. Infected/activated MP initiate neuroinflammation activating glial cells and ultimately disrupting neuronal function. Astrocytes secrete tissue inhibitor of metalloproteinase (TIMP)-1 in response to neural injury. Altered TIMP-1 levels are implicated in several CNS diseases. CCAAT enhancer-binding protein β (C/EBPβ), a transcription factor, is expressed in rodent brains in response to neuroinflammation, implicating it in Alzheimer's, Parkinson's, and HAND. Here, we report that C/EBPβ mRNA levels are elevated and its isoforms differentially expressed in total brain tissue lysates of HIV-1-infected and HIV-1 encephalitis patients. In vitro, HAND-relevant stimuli additively induce C/EBPβ nuclear expression in human astrocytes through 7 days of treatment. Over-expression of C/EBPβ increases TIMP-1 promoter activity, mRNA, and protein levels in human astrocytes activated with interleukin-1β. Knockdown of C/EBPβ with siRNA decreases TIMP-1 mRNA and protein levels. These data suggest that C/EBPβ isoforms are involved in complex regulation of astrocyte TIMP-1 production during HIV-1 infection; however, further studies are required to completely understand their role during disease progression.
    Keywords: Astrocytes -- Metabolism ; Brain -- Pathology ; Ccaat-Enhancer-Binding Protein-Beta -- Metabolism ; Gene Expression Regulation -- Physiology ; HIV Infections -- Pathology ; Tissue Inhibitor of Metalloproteinase-1 -- Metabolism
    ISSN: 00223042
    E-ISSN: 1471-4159
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  • 2
    Language: English
    In: mBio, 01 November 2018, Vol.9(6), p.e02100-18
    Description: The alphaproteobacterium Agrobacterium tumefaciens is able to infect various eudicots causing crown gall tumor formation. Based on its unique ability of interkingdom gene transfer, Agrobacterium serves as a crucial biotechnological tool for genetic manipulation of plant cells. The presence of hundreds of putative sRNAs in this organism suggests a considerable impact of riboregulation on A. tumefaciens physiology. Here, we characterized the biological function of the sRNA PmaR that controls various processes crucial for growth, motility, and virulence. Among the genes directly targeted by PmaR is ampC coding for a beta-lactamase that confers ampicillin resistance, suggesting that the sRNA is crucial for fitness in the competitive microbial composition of the rhizosphere.Small regulatory RNAs play an important role in the adaptation to changing conditions. Here, we describe a differentially expressed small regulatory RNA (sRNA) that affects various cellular processes in the plant pathogen Agrobacterium tumefaciens. Using a combination of bioinformatic predictions and comparative proteomics, we identified nine targets, most of which are positively regulated by the sRNA. According to these targets, we named the sRNA PmaR for peptidoglycan biosynthesis, motility, and ampicillin resistance regulator. Agrobacterium spp. are long known to be naturally resistant to high ampicillin concentrations, and we can now explain this phenotype by the positive PmaR-mediated regulation of the beta-lactamase gene ampC. Structure probing revealed a spoon-like structure of the sRNA, with a single-stranded loop that is engaged in target interaction in vivo and in vitro. Several riboregulators have been implicated in antibiotic resistance mechanisms, such as uptake and efflux transporters, but PmaR represents the first example of an sRNA that directly controls the expression of an antibiotic resistance gene.
    Keywords: Antibiotic Resistance ; Gene Regulation ; Plant-Microbe Interaction ; Posttranscriptional Control ; Regulatory RNA ; Biology
    ISSN: 21612129
    E-ISSN: 2150-7511
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  • 3
    In: Molecular psychiatry, 2015, Vol.20(9), p.1091-1100
    Description: Numerous investigations support decreased glutamatergic signaling as a pathogenic mechanism of schizophrenia: yet molecular underpinnings for such dysregulation are largely unknown. In the postmortem dorsolateral prefrontal cortex, we found striking decreases in tyrosine phosphorylation of N-methyl-D aspartate (NMDA) receptor subunit 2 (GluN2), which is critical for neuroplasticity. The decreased GluN2 activity in schizophrenia may not be due to downregulation of NMDA receptors since MK-801 binding and NMDA receptor complexes in the PSD were in fact increased in schizophrenia cases. At the post-receptor level, however, we found striking reductions in the protein kinase C, Pyk 2 and Src kinase activity, which in tandem can decrease GluN2 activation. Given that Src serves as a hub of various signaling mechanisms impacting GluN2 phosphorylation, we postulated that Src hypoactivity may result from convergent alterations of various schizophrenia susceptibility pathways and thus mediate their impacts on NMDA receptor signaling. Indeed, the DLPFC of schizophrenia cases exhibit increased PSD-95 and erbB4 and decreased RPTPa and dysbindin-1, each of which reduces Src activity via protein interaction with Src. To test genomic underpinnings for Src hypoactivity, we examined genome wide association study results, incorporating 13,394 cases and 34,676 controls, which yielded no significant association of individual variants of Src and its direct regulators with schizophrenia. However, a wider protein-protein interaction based network centered on Src, showed significant enrichment of gene-level associations with schizophrenia compared to other psychiatric illnesses. Our results together demonstrate striking decreases in NMDA receptor signaling at the post-receptor level and propose Src as a nodal point of convergent dysregulations impacting NMDA receptor pathway via protein-protein associations.
    Keywords: Article ; Nmda Receptor ; Postsynaptic Density ; Postmortem Brain ; Nmdar Hypofunction ; Src Kinase
    ISSN: 1359-4184
    E-ISSN: 1476-5578
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  • 4
    Language: English
    In: Journal of neuroscience research, 15 May 2006, Vol.83(7), pp.1271-80
    Description: Astrocyte production of tissue inhibitor of metalloproteinase (TIMP)-1 is important in central nervous system (CNS) homeostasis and inflammatory diseases such as HIV-1-associated dementia (HAD). TIMPs and matrix metalloproteinases (MMPs) regulate the remodeling of the extracellular matrix. An imbalance between TIMPs and MMPs is associated with many pathologic conditions. Our recently published studies uniquely demonstrate that HAD patients have reduced levels of TIMP-1 in the brain. Astrocyte-TIMP-1 expression is differentially regulated in acute and chronic inflammatory conditions. In this and the adjoining report (Gardner et al., 2006), we investigate the mechanisms that may be involved in differential TIMP-1 regulation. One mechanism for TIMP-1 downregulation is the production of anti-inflammatory molecules, which can activate signaling pathways during chronic inflammation. We investigated the contribution of transforming growth factor (TGF)-signaling in astrocyte-MMP/TIMP-1-astrocyte regulation. TGF-beta1 and beta2 levels were upregulated in HAD brain tissues. Co-stimulation of astrocytes with IL-1beta and TGF-beta mimicked the TIMP-1 downregulation observed with IL-1beta chronic activation. Measurement of astrocyte-MMP protein levels showed that TGF-beta combined with IL-1beta increased MMP-2 and decreased proMMP-1 expression compared to IL-1beta alone. We propose that one of the mechanisms involved in TIMP-1 downregulation may be through TGF-signaling in chronic immune activation. These studies show a novel extracellular regulatory loop in astrocyte-TIMP-1 regulation.
    Keywords: AIDS Dementia Complex -- Metabolism ; Astrocytes -- Metabolism ; Brain -- Metabolism ; Encephalitis -- Metabolism ; Tissue Inhibitor of Metalloproteinase-1 -- Metabolism ; Transforming Growth Factor Beta -- Metabolism
    ISSN: 0360-4012
    E-ISSN: 10974547
    Source: MEDLINE/PubMed (U.S. National Library of Medicine)
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  • 5
    Language: English
    In: Journal of Neuroscience Research, 15 May 2006, Vol.83(7), pp.1271-1280
    Description: Astrocyte production of tissue inhibitor of metalloproteinase (TIMP)‐1 is important in central nervous system (CNS) homeostasis and inflammatory diseases such as HIV‐1‐associated dementia (HAD). TIMPs and matrix metalloproteinases (MMPs) regulate the remodeling of the extracellular matrix. An imbalance between TIMPs and MMPs is associated with many pathologic conditions. Our recently published studies uniquely demonstrate that HAD patients have reduced levels of TIMP‐1 in the brain. Astrocyte‐TIMP‐1 expression is differentially regulated in acute and chronic inflammatory conditions. In this and the adjoining report (Gardner et al., 2006), we investigate the mechanisms that may be involved in differential TIMP‐1 regulation. One mechanism for TIMP‐1 downregulation is the production of anti‐inflammatory molecules, which can activate signaling pathways during chronic inflammation. We investigated the contribution of transforming growth factor (TGF)‐signaling in astrocyte‐MMP/TIMP‐1‐astrocyte regulation. TGF‐β1 and β2 levels were upregulated in HAD brain tissues. Co‐stimulation of astrocytes with IL‐1β and TGF‐β mimicked the TIMP‐1 downregulation observed with IL‐1β chronic activation. Measurement of astrocyte‐MMP protein levels showed that TGF‐β combined with IL‐1β increased MMP‐2 and decreased proMMP‐1 expression compared to IL‐1β alone. We propose that one of the mechanisms involved in TIMP‐1 downregulation may be through TGF‐signaling in chronic immune activation. These studies show a novel extracellular regulatory loop in astrocyte‐TIMP‐1 regulation. © 2006 Wiley‐Liss, Inc.
    Keywords: Transforming Growth Factor ; Neurodegeneration ; Chronic Inflammation ; Hiv‐1‐Associated Dementia ; Extracellular Matrix ; Astrocyte‐Activation
    ISSN: 0360-4012
    E-ISSN: 1097-4547
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  • 6
    Language: English
    In: Journal of Neuroscience Research, 15 May 2006, Vol.83(7), pp.1281-1292
    Description: The pathogenesis of many neurodegenerative disorders, including human immunodeficiency virus (HIV)‐1 associated dementia, is exacerbated by an imbalance between matrix metalloproteinases (MMPs) and their inhibitors, tissue inhibitors of metalloproteinases (TIMPs). In the context of disease, TIMP‐1 has emerged as an important multifunctional protein capable of regulating inflammation. We previously reported differential TIMP‐1 expression in acute versus chronic activation of astrocytes. This study investigates possible mechanisms underlying TIMP‐1 downregulation in chronic neuroinflammation. We used interleukin (IL)‐1β as a model pro‐inflammatory stimulus and measured TIMP‐1 binding to extracellular matrix, cell death, receptor downregulation, TIMP‐1 mRNA stability and transcriptional regulation in activated astrocytes. TIMP‐1 remained localized to the cell body or was secreted into the cell supernatant. DNA fragmentation ELISA and MTT assay showed that prolonged IL‐1β activation of astrocytes induced significant astrocyte death. In acute and chronic IL‐1β‐activated astrocytes, IL‐1 receptor levels were not significantly different. TIMP‐1 mRNA stability was measured in astrocytes and U87 astroglioma cells by real‐time PCR, and TIMP‐1 promoter activation was studied using TIMP‐1‐luciferase reporter constructs in transfected astrocytes. Our results indicated that TIMP‐1 expression is regulated through multiple mechanisms. Transcriptional control and loss of mRNA stabilization are, however, the most likely primary contributors to chronic downregulation of TIMP‐1. These data are important for unraveling the mechanisms underlying astrocyte responses during chronic neuroinflammation and have broader implications in other inflammatory diseases that involve MMP/TIMP imbalance. © 2006 Wiley‐Liss, Inc.
    Keywords: Timp‐1 ; Il‐1β ; Neurodegenerative Disorders ; Hiv‐1
    ISSN: 0360-4012
    E-ISSN: 1097-4547
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  • 7
    Language: English
    In: CyTA - Journal of Food, 01 January 2019, Vol.17(1), pp.20-24
    Description: Soy derivatives contain isoflavones with structural similarity to estrogen hormones known as phytoestrogens. The levels of isoflavones in these foods are quite variable and often unknown. The objective of this work was to develop and validate a methodology for the quantification of isoflavone genistein in soymilk by liquid chromatography coupled with an ultraviolet detector. After quantifying the levels of genistein in soymilk, the behavioral effects of daily administration of soymilk supplemented or not with glyphosate (50 or 100 mg/kg) throughout the pre-pubertal period in male rats were evaluated. The method developed is selective, sensitive, specific, and precise for the quantification of genistein with a total execution time of 20 min. Behavioral test highlights changes in anxiety pattern after chronic prepubertal exposure to soymilk containing 26.46 μg/mL genistein.
    Keywords: Hplc ; Soymilk ; Isoflavones ; Phytoestrogens ; Anxiety ; Genistein ; Hplc (Cromatografía de Alta Resolución En Fase Líquida) ; Leche de Soya ; Isoflavonas ; Fitoestrógenos ; Ansiedad ; Genisteína ; Diet & Clinical Nutrition
    ISSN: 1947-6337
    E-ISSN: 1947-6345
    Source: Taylor & Francis (Taylor & Francis Group)
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