Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Lammers, B; Chandak, PG; Aflaki, E; Van Puijvelde, GH; Radovic, B; Hildebrand, RB; Meurs, I; Out, R; Kuiper, J; Van Berkel, TJ; Kolb, D; Haemmerle, G; Zechner, R; Levak-Frank, S; Van Eck, M; Kratky, D.
Macrophage adipose triglyceride lipase deficiency attenuates atherosclerotic lesion development in low-density lipoprotein receptor knockout mice.
Arterioscler Thromb Vasc Biol. 2011; 31(1): 67-73. [OPEN ACCESS]
Web of Science PubMed PUBMED Central FullText FullText_MUG


Autor/innen der Med Uni Graz:
Aflaki Elma
Chandak Prakash Gopal Das
Kolb-Lenz Dagmar
Kratky Dagmar
Levak Sanja
Radovic Branislav

Dimensions Citations:

Plum Analytics:
Number of Figures: 5
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Objective-The consequences of macrophage triglyceride (TG) accumulation on atherosclerosis have not been studied in detail so far. Adipose triglyceride lipase (ATGL) is the rate-limiting enzyme for the initial step in TG hydrolysis. Because ATGL knockout (KO) mice exhibit massive TG accumulation in macrophages, we used ATGL KO mice to study the effects of macrophage TG accumulation on atherogenesis. Methods and Results-Low-density lipoprotein receptor (LDLr) KO mice were transplanted with bone marrow from ATGL KO (ATGL KO -> LDLr KO) or wild-type (WT -> LDLr KO) mice and challenged with a Western-type diet for 9 weeks. Despite TG accumulation in ATGL KO macrophages, atherosclerosis in ATGL KO -> LDLr KO mice was 43% reduced associated with decreased plasma monocyte chemoattractant protein-1 (MCP-1) and macrophage interleukin-6 concentrations. This coincided with a reduced amount of macrophages, possibly because of a 39% increase in intraplaque apoptosis and a decreased migratory capacity of ATGL KO macrophages. The reduced number of white blood cells might be due to a 36% decreased Lin(-)Sca-1(+)cKit(+) hematopoietic stem cell population. Conclusion-We conclude that the attenuation of atherogenesis in ATGL KO -> LDLr KO mice is due to decreased infiltration of less inflammatory macrophages into the arterial wall and increased macrophage apoptosis. (Arterioscler Thromb Vasc Biol. 2011;31:67-73.)
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Apoptosis -
Atherosclerosis - enzymology
Bone Marrow Transplantation -
Carboxylic Ester Hydrolases - deficiency
Cells, Cultured -
Chemokine CCL2 - blood
Chemotaxis -
Cholesterol - blood
Diet, Atherogenic -
Disease Models, Animal -
Female -
Gene Expression Regulation -
Hematopoietic Stem Cells - metabolism
Hydrolysis -
Inflammation Mediators - metabolism
Interleukin-6 - metabolism
Leukocyte Count -
Lipase -
Macrophages - enzymology
Male -
Mice -
Mice, Knockout -
Multipotent Stem Cells - metabolism
Receptors, LDL - deficiency
Triglycerides - blood
Whole-Body Irradiation -

Find related publications in this database (Keywords)
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