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Lubeseder-Martellato, C. ; Guenzi, E. ; Jörg, A. ; Töpolt, K. ; Naschberger, E. ; Kremmer, E. ; Zietz, C.* ; Tschachler, E.* ; Hutzler, P. ; Schwemmle, M.* ; Matzen, K. ; Grimm, Th. ; Ensoli, B.*

Guanylate-Binding Protein-1 Expression is Selectively Induced by Inflammatory Cytokines and is an Activation Marker of Endothelial Cells during Inflammatory Diseases.

Am. J. Pathol. 161, 1749-1759 (2002)
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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-a, 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.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter ANGIOGENESIS IN-VITRO; TUMOR-NECROSIS-FACTOR; GAMMA-INTERFERON; GROWTH-FACTOR; KAPOSIS-SARCOMA; ADHESION MOLECULE-1; SPINDLE CELLS; VASCULAR-PERMEABILITY; NUCLEOTIDE-BINDING; GENE-EXPRESSION
Sprache englisch
Veröffentlichungsjahr 2002
HGF-Berichtsjahr 2002
ISSN (print) / ISBN 0002-9440
e-ISSN 1525-2191
Quellenangaben Band: 161, Heft: 5, Seiten: 1749-1759 Artikelnummer: , Supplement: ,
Verlag Elsevier
Begutachtungsstatus Peer reviewed
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease

Forschungsfeld(er) Enabling and Novel Technologies

Immune Response and Infection
PSP-Element(e) G-500300-001
G-501700-003
FE 72731
Erfassungsdatum 2002-11-12