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  1. Book ; Online ; Thesis: Untersuchungen zur Rolle des HIV-1-Tat-Proteins in der AIDS-assoziierten Vaskulopathie

    Matzen, Kathrin

    2003  

    Author's details vorgelegt von Kathrin Matzen
    Language German
    Size Online-Ressource
    Document type Book ; Online ; Thesis
    Thesis / German Habilitation thesis Univ., Diss--München, 2003
    Database Former special subject collection: coastal and deep sea fishing

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  2. Book ; Online ; Thesis: Untersuchungen zur Rolle des HIV-1-Tat-Proteins in der AIDS-assoziierten Vaskulopathie

    Matzen, Kathrin [Verfasser]

    2003  

    Author's details vorgelegt von Kathrin Matzen
    Keywords Medizin, Gesundheit ; Medicine, Health
    Subject code sg610
    Document type Book ; Online ; Thesis
    Database Digital theses on the web

    Full text online

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  3. Article: RNase H-mediated retrovirus destruction in vivo triggered by oligodeoxynucleotides.

    Matzen, Kathrin / Elzaouk, Lina / Matskevich, Alexey A / Nitzsche, Anja / Heinrich, Jochen / Moelling, Karin

    Nature biotechnology

    2007  Volume 25, Issue 6, Page(s) 669–674

    Abstract: The HIV-1 RNase H can be prematurely activated by oligodeoxynucleotides targeting the highly conserved polypurine tract required for second strand DNA synthesis. This inhibits retroviral replication in cell-free HIV particles and newly infected cells. ... ...

    Abstract The HIV-1 RNase H can be prematurely activated by oligodeoxynucleotides targeting the highly conserved polypurine tract required for second strand DNA synthesis. This inhibits retroviral replication in cell-free HIV particles and newly infected cells. Here we extend these studies to an in vivo model of retroviral replication. Mice that are chronically infected with the spleen focus-forming virus and treated with oligodeoxynucleotides that target the polypurine tract, exhibit either transient or long-term reductions in plasma virus titer, depending on the therapeutic regimen. Treatment prior to, during or shortly after infection can delay disease progression, increase survival rates and prevent viral infection. This strategy destroys viral RNA template in virus particles in serum as well as early retroviral replication intermediates in infected cells. As it targets events common to the replication cycle of all retroviruses, this approach may be broadly applicable to retroviruses of medical and agricultural importance.
    MeSH term(s) Animals ; Gene Silencing ; Gene Targeting/methods ; HIV Infections/genetics ; HIV Infections/therapy ; HIV Infections/virology ; HIV-1/genetics ; Mice ; NIH 3T3 Cells ; Retroviridae/genetics ; Ribonuclease H/genetics
    Chemical Substances Ribonuclease H (EC 3.1.26.4)
    Language English
    Publishing date 2007-06
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1311932-1
    ISSN 1546-1696 ; 1087-0156
    ISSN (online) 1546-1696
    ISSN 1087-0156
    DOI 10.1038/nbt1311
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2167: Show issues Location:
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  4. Article: HIV-1 Tat increases the adhesion of monocytes and T-cells to the endothelium in vitro and in vivo: implications for AIDS-associated vasculopathy.

    Matzen, Kathrin / Dirkx, Anita E M / oude Egbrink, Mirjam G A / Speth, Cornelia / Götte, Matthias / Ascherl, Gudrun / Grimm, Thomas / Griffioen, Arjan W / Stürzl, Michael

    Virus research

    2004  Volume 104, Issue 2, Page(s) 145–155

    Abstract: HIV-1-infected patients exhibit severe damages of the aortic endothelium, develop angioproliferative lesions such as Kaposi's sarcoma (KS), and have an increased risk of cardiovascular diseases and atherosclerosis. An increased adhesion of leukocytes to ... ...

    Abstract HIV-1-infected patients exhibit severe damages of the aortic endothelium, develop angioproliferative lesions such as Kaposi's sarcoma (KS), and have an increased risk of cardiovascular diseases and atherosclerosis. An increased adhesion of leukocytes to the endothelium is a common pathogenic parameter of AIDS-associated vascular diseases. Here we show that the HIV-1 Tat protein, a regulatory protein of HIV-1 released by infected cells, and TNF-alpha, a cytokine increased in sera and tissues of HIV-1-infected patients, activate synergistically the adhesion of leukocytes to endothelial cells both in vitro and in vivo. This effect is selectively mediated by HIV-1 Tat, since HIV-1 Nef, another HIV-1 regulatory protein, and the HIV-1 envelope protein gp41, had no effect. In vitro adhesion assays with PBMC and quantitative cell type analysis of adherent cells by FACS demonstrated that HIV-1 Tat selectively activates the adhesion of T-cells and monocytes but not of B-cells. Intravital microscopic studies in mice confirmed the synergistic activity of HIV-1 Tat and TNF-alpha on leukocyte adhesion to the endothelium in vivo. These data indicate that HIV-1 Tat in cooperation with TNF-alpha may contribute to the vascular damage and cardiovascular diseases observed in AIDS patients but also to the prominent extravasation of T-cells and monocytes which is a key process in the formation and progression of KS lesions.
    MeSH term(s) Cell Adhesion/drug effects ; Cell Adhesion/physiology ; Cell Aggregation ; Cells, Cultured ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/immunology ; Gene Products, tat/immunology ; Gene Products, tat/pharmacology ; HIV-1/chemistry ; Humans ; In Vitro Techniques ; Monocytes/drug effects ; Monocytes/immunology ; RNA, Messenger ; Receptors, Cytoadhesin/metabolism ; T-Lymphocytes/drug effects ; T-Lymphocytes/immunology ; Tumor Necrosis Factor-alpha/immunology ; tat Gene Products, Human Immunodeficiency Virus
    Chemical Substances Gene Products, tat ; RNA, Messenger ; Receptors, Cytoadhesin ; Tumor Necrosis Factor-alpha ; tat Gene Products, Human Immunodeficiency Virus
    Language English
    Publishing date 2004-09-01
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 605780-9
    ISSN 1872-7492 ; 0168-1702
    ISSN (online) 1872-7492
    ISSN 0168-1702
    DOI 10.1016/j.virusres.2004.04.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1965: Show issues Location:
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  5. Article: Guanylate-binding protein-1 expression is selectively induced by inflammatory cytokines and is an activation marker of endothelial cells during inflammatory diseases.

    Lubeseder-Martellato, Clara / Guenzi, Eric / Jörg, Anita / Töpolt, Kristin / Naschberger, Elisabeth / Kremmer, Elisabeth / Zietz, Christian / Tschachler, Erwin / Hutzler, Peter / Schwemmle, Martin / Matzen, Kathrin / Grimm, Thomas / Ensoli, Barbara / Stürzl, Michael

    The American journal of pathology

    2002  Volume 161, Issue 5, Page(s) 1749–1759

    Abstract: During angiogenesis and inflammatory processes, endothelial cells acquire different activation phenotypes, whose identification may help in understanding the complex network of angiogenic and inflammatory interactions in vivo. To this goal we ... ...

    Abstract During angiogenesis and inflammatory processes, endothelial cells acquire different activation phenotypes, whose identification may help in understanding the complex network of angiogenic and inflammatory interactions in vivo. To this goal we investigated the expression of the human guanylate-binding protein (GBP)-1 that is highly induced by inflammatory cytokines (ICs) and, therefore, may characterize IC-activated cells. Using a new rat monoclonal antibody raised against GBP-1, we show that GBP-1 is a cytoplasmic protein and that its expression in endothelial cells is selectively induced by interferon-gamma, interleukin-1alpha, interleukin-1beta, or tumor necrosis factor-alpha, but not by other cytokines, chemokines, or growth factors. Moreover, we found that GBP-1 expression is highly associated with vascular endothelial cells as confirmed by the simultaneous detection of GBP-1 and the endothelial cell-associated marker CD31 in a broad range of human tissues. Notably, GBP-1 expression was undetectable in the skin, but it was highly induced in vessels of skin diseases with a high-inflammatory component including psoriasis, adverse drug reactions, and Kaposi's sarcoma. These results indicate that GBP-1 is a novel cellular activation marker that characterizes the IC-activated phenotype of endothelial cells.
    MeSH term(s) Biomarkers/analysis ; Cell Line ; Cells, Cultured ; Cytokines/pharmacology ; DNA-Binding Proteins/biosynthesis ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/metabolism ; GTP-Binding Proteins/biosynthesis ; Humans ; Inflammation/blood ; Inflammation/metabolism ; Interferon-gamma/pharmacology ; Psoriasis/blood ; Psoriasis/metabolism ; Sarcoma, Kaposi/blood supply ; Sarcoma, Kaposi/metabolism ; Skin Diseases/blood ; Skin Diseases/immunology ; Skin Diseases/metabolism ; Tissue Distribution
    Chemical Substances Biomarkers ; Cytokines ; DNA-Binding Proteins ; GBP1 protein, human ; Interferon-gamma (82115-62-6) ; GTP-Binding Proteins (EC 3.6.1.-)
    Language English
    Publishing date 2002-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/S0002-9440(10)64452-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Ud II Zs.76: Show issues Location:
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