| Summary: | Oxidised low-density lipoproteins and cyclopentenone prostaglandin accelerated monocyte apoptosis, in serum-free conditions, in a concentration dependent manner. Cyclopentenone prostaglandin-induced monocyte apoptosis was caspase dependent, but oxidised low-density lipoprotein-induced monocyte apoptosis only partially caspase-dependent. Monocyte apoptosis appeared to be independent of the nuclear receptor and transcriptional controlled peroxisome proliferator receptor gamma PPARγ. Arachidonate-induced monocyte apoptosis appeared to be caused by a disruption of NF-κB mediated signalling. Monocyte apoptosis appeared inversely related to maturation, with naïve undifferentiated monocytes being more susceptible to programmed cell death than committed macrophages. Monocyte transcriptional responses to oxidised LDL were assessed using gene mini-arrays. Genes for CD47 and CD11a showed significant levels of variation on the array. Monocyte surface molecular changes induced by low-density lipoprotein were directly assessed by indirect immuno-labelling and flow cytometric analysis. Oxidised low-density lipoprotein elevated monocyte surface CD54 in early suspension culture, but then caused a down-regulation of CD54 in prolonged adherent culture. Oxidised low-density lipoprotein diminished monocyte surface expression of CD11b and CD11c in a manner dependent upon adhesion and maturation. CD49d expression appeared to be reduced by oxidised low-density lipoprotein in mature adherent monocytes. Early marginal reductions in CD11a expression were not seen in more mature monocytes. These findings may contribute to our understanding of cell death in atherosclerotic lesions, and potential limitations on cell mobility out of atherosclerotic plaque.
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