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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Schlager, S; Goeritzer, M; Jandl, K; Frei, R; Vujic, N; Kolb, D; Strohmaier, H; Dorow, J; Eichmann, TO; Rosenberger, A; Wölfler, A; Lass, A; Kershaw, EE; Ceglarek, U; Dichlberger, A; Heinemann, A; Kratky, D.
Adipose triglyceride lipase acts on neutrophil lipid droplets to regulate substrate availability for lipid mediator synthesis.
J Leukoc Biol. 2015; 98(5):837-850 [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Frei-Winterleitner Robert
Göritzer Madeleine
Heinemann Akos
Jandl Katharina
Kolb-Lenz Dagmar
Kratky Dagmar
Rosenberger Angelika
Schlager Stefanie
Strohmaier Heimo
Vujic Nemanja
Wölfler Albert

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Plum Analytics:
Number of Figures: 9
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In humans, mutations in ATGL lead to TG accumulation in LDs of most tissues and cells, including peripheral blood leukocytes. This pathologic condition is called Jordans' anomaly, in which functional consequences have not been investigated. In the present study, we tested the hypothesis that ATGL plays a role in leukocyte LD metabolism and immune cell function. Similar to humans with loss-of-function mutations in ATGL, we found that global and myeloid-specific Atgl(-/-) mice exhibit Jordans' anomaly with increased abundance of intracellular TG-rich LDs in neutrophil granulocytes. In a model of inflammatory peritonitis, lipid accumulation was also observed in monocytes and macrophages but not in eosinophils or lymphocytes. Neutrophils from Atgl(-/-) mice showed enhanced immune responses in vitro, which were more prominent in cells from global compared with myeloid-specific Atgl(-/-) mice. Mechanistically, ATGL(-/-) as well as pharmacological inhibition of ATGL led to an impaired release of lipid mediators from neutrophils. These findings demonstrate that the release of lipid mediators is dependent on the liberation of precursor molecules from the TG-rich pool of LDs by ATGL. Our data provide mechanistic insights into Jordans' anomaly in neutrophils and suggest that ATGL is a potent regulator of immune cell function and inflammatory diseases. © The Author(s).
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Humans -
Lipase - genetics
Lipase - metabolism
Lipid Droplets - enzymology
Lipid Droplets - pathology
Lipid Metabolism -
Lipid Metabolism Disorders - enzymology
Lipid Metabolism Disorders - genetics
Lipid Metabolism Disorders - pathology
Lymphocytes - enzymology
Lymphocytes - pathology
Mice -
Mice, Knockout -
Monocytes - enzymology
Monocytes - pathology
Neutrophils - enzymology
Neutrophils - pathology
Peritonitis - enzymology
Peritonitis - genetics
Peritonitis - pathology

Find related publications in this database (Keywords)
inflammatory cells
arachidonic acid
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