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1 downregulates CD36 and scavenger receptor A but
upregulates LOX-1 in human macrophages
Institut für Prophylaxe und Epidemiologie der Kreislaufkrankheiten, Universität München, 81245 Munich, Germany
Transforming growth factor-
1 (TGF-1), a key
cytokine for control of cell growth, extracellular matrix formation,
and inflammation control, is secreted by many cells present in the
arteriosclerotic plaque. Lipid accumulation in the vessel wall is
regarded as an early step in atherogenesis and depends on uptake of
modified low-density lipoprotein (LDL) by macrophages through scavenger receptors and their transformation into foam cells. Prominent members
of the scavenger receptor family are the class A type I and II
receptors (ScR-A), the class B receptor CD36, and the recently detected
lectin-like oxidized LDL receptor-1 (LOX-1), which, unlike the native
LDL receptor (LDL-R), are not feedback controlled. CD36 is responsible
for >50% of modified LDL uptake into human monocyte-derived
macrophages. We therefore studied whether TGF-1 influences
expression and function of ScR-A, CD36, and LOX-1 in monocytes using
RT-PCR and flow cytometry. Total uptake of oxidized LDL by monocytoid
cells, reflecting the combined function of all scavenger receptors, was
significantly reduced by TGF-1. At initially low picomolar
concentrations, TGF-1 decreased CD36 mRNA and protein surface
expression and ScR-A mRNA levels in the human monocytic cell line THP-1
and in freshly isolated and cultivated human monocytes, whereas LOX-1
mRNA was increased. Expression of LDL-R and -actin was not affected
by TGF-1. In conclusion, depression of scavenger receptor function
in monocytes by TGF-1 in low concentrations reduces foam cell
formation. Together with matrix control by TGF-1, this may be
important for atherogenesis and plaque stabilization.
transforming growth factor-1; scavenger receptor class
A
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