Letters to the Editor |
Arthritis and Inflammation Research Centre, University of Melbourne, Department of Medicine, The Royal Melbourne Hospital, Parkville, Victoria, Australia, 3050
Heart Research Institute, Camperdown, New South Wales, Australia
To the Editor:
It is likely that in the early stages of atherosclerosis, circulating monocytes migrate into the subendothelial space, where they can mature into foam cells.1 2 3 4 5 There is in vivo and in vitro evidence for both foam cell death but also enhanced survival and growth.6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22
Human peripheral blood monocytes (
95% pure) were
obtained by countercurrent elutriation and usually cultured in minimal
essential medium,
-modification (
-MEM)/1% pooled normal human
serum (HS).23 24 The number of viable cells was measured
by scraping the tissue culture surface and counting them in a
hemocytometer with trypan blue exclusion or by propidium iodide
staining (flow cytometry). Oxidized LDL (ox-LDL) was prepared as
before.14
The number of viable monocytes declined when they were
left untreated or treated with native LDL; this loss was reduced by
both ox-LDL and acetylated LDL (ac-LDL; see the
Table
). A dose response for the
ox-LDL effect is provided in the online Figure
(please see http://atvb.ahajournals.org)
and, as we found before with murine macrophages,14
doses of ox-LDL
50 µg/mL generally promoted survival; at these
survival-inducing doses, the cells spread on the tissue culture surface
and remained attached. In contrast, at higher concentrations, viable
cell numbers again declined. With different ox-LDL preparations, the
effective survival dose response varied to some extent. The ability of
ox-LDL to enhance human monocyte survival was confirmed with monocytes
from 30 donors. We previously found that prior adherence of the
monocytes for a short period under serum-free conditions, followed by
culture in 1% HS, improved
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