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E-GEOD-6054 - Transcription profiling by array of human circulating monocytes from patients with familial hypercholesterolemia, homozygous or heterozygous mutant for LDLR

Released on 14 June 2008, last updated on 8 May 2012
Homo sapiens
Samples (25)
Array (1)
Protocols (5)
Atherosclerosis is the major cause of death in industrialized countries. This disease has initially been characterized as a lipid disorder, but current concepts argue for an inflammatory disease, which develops in the background of hypercholesterolemia and other risk factors. In response to initial events of atherosclerosis formation, such as LDL-deposition in the subendothelial space, monocytes and T cells interact with the vessel wall. However, little is known about the properties and the behavior of these cells in this context. Using familial hypercholesterolemia (FH) as a model we demonstrate substantial differences in the gene expression of freshly isolated human monocytes and T lymphocytes. In FH monocytes we found an increased uptake of oxidized LDL, elevated amounts of scavenger receptors and adhesion molecules, and differences in the regulation of intracellular lipoprotein metabolism compared to monocytes from healthy individuals. Furthermore, the monocyte subpopulation of CD14+/CD16+ cells is less frequent in FH but exhibits significantly higher levels of CD11c and CD29 which increases the likelihood for their transmigration through the endothelial layer. The presence of increased amounts of CD69 in T lymphocytes from FH patients suggests that these cells are more activated than control cells. Our results indicate that some important steps of atherosclerosis formation already take place in circulating blood cells which extends current atherosclerosis models to the plasma compartment. Experiment Overall Design: 25 monocytes samples: 5 homozygous FH, 7 heterozygous FH, 13 control participants
Experiment types
transcription profiling by array, unknown experiment type
Monocytes of patients with familial hypercholesterolemia show alterations in cholesterol metabolism. Mosig S, Rennert K, Büttner P, Krause S, Lütjohann D, Soufi M, Heller R, Funke H. , PMID:19040724
Investigation descriptionE-GEOD-6054.idf.txt
Sample and data relationshipE-GEOD-6054.sdrf.txt
Raw data (2),
Processed data (1)
Array designA-AFFY-44.adf.txt
R ExpressionSetE-GEOD-6054.eSet.r