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Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Popovic, ZV; Sandhoff, R; Sijmonsma, TP; Kaden, S; Jennemann, R; Kiss, E; Tone, E; Autschbach, F; Platt, N; Malle, E; Gröne, HJ.
Sulfated glycosphingolipid as mediator of phagocytosis: SM4s enhances apoptotic cell clearance and modulates macrophage activity.
J Immunol. 2007; 179(10): 6770-6782. [OPEN ACCESS]
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Autor/innen der Med Uni Graz:
Malle Ernst
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Number of Figures: 10
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Abstract:
Sulfoglycolipids are present on the surface of a variety of cells. The sulfatide SM4s is increased in lung, renal, and colon cancer and is associated with an adverse prognosis, possibly due to a low immunoreactivity of the tumor. As macrophages significantly contribute to the inflammatory infiltrate in malignancies, we postulated that SM4s may modulate macrophage function. We have investigated the effect of SM4s on the uptake of apoptotic tumor cells, macrophage cytokine profile, and receptor expression. Using flow cytometry and microscopic analyses, we found that coating apoptotic murine carcinoma cells from the colon and kidney with SM4s promoted their phagocytosis by murine macrophages up to 3-fold ex vivo and in vivo. This increased capacity was specifically inhibited by preincubation of macrophages with oxidized or acetylated low density lipoprotein and maleylated albumin, indicating involvement of scavenger receptors in this interaction. The uptake of SM4s-coated apoptotic cells significantly enhanced macrophage production of TGF-beta1, expression of P-selectin, and secretion of IL-6. These data suggest that SM4s within tumors may promote apoptotic cell removal and alter the phenotype of tumor-associated macrophages.
Find related publications in this database (using NLM MeSH Indexing)
Albumins - pharmacology
Animals - pharmacology
Apoptosis - drug effects
Cell Line, Tumor - drug effects
Colonic Neoplasms - metabolism
Glycolipids - metabolism
Humans - metabolism
Inflammation - metabolism
Interleukin-6 - biosynthesis
Kidney Neoplasms - metabolism
Lipoproteins, LDL - pharmacology
Lung Neoplasms - metabolism
Macrophages - metabolism
Mice - metabolism
Mice, Inbred BALB C - metabolism
Monokines - biosynthesis
P-Selectin - biosynthesis
Prognosis - biosynthesis
Receptors, Scavenger - agonists
Transforming Growth Factor beta1 - biosynthesis
Tumor Markers, Biological - metabolism

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