Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 377, Issue 2, Pages 484-488Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2008.09.140
Keywords
Macrophage proliferation; Native LDL; Oxidized LDL; Acetylated LDL; Cholesterol; Desmosterol; Lovastatin; Mevalonate; Hydroxymethyl glutaryl coenzyme A reductase
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Funding
- Fondo de Investigacion Sanitaria [00/0229]
- Ministerio de Ciencia y Tecnologia [BMC2002-01262]
- Ministerio de Educacion y Ciencia [SAF2005-07038]
- Instituto de Salud Carlos III
- Comunidad Autonoma de Madrid
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We addressed the ability of native, oxidized and acetylated low-density lipoproteins (nLDL, oxLDL and acLDL, respectively) and desmosterol to act as sources of sterol for the Proliferation of J774A.1 macrophages, Treatment with 0.5 mu M lovastatin and lipoprotein-deficient serum suppressed cell proliferation. This inhibition was effectively prevented by nLDL, but only to a lesser extent by oxLDL. AcLDL, despite its ability to deliver a higher amount of cholesterol to J774 macrophages than the other LDLs, was dependent on mevalonate supply to sustain cell proliferation. Similarly, exogenous desmosterol which is not converted into cholesterol in, J774 cells, required the simultaneous addition of mevalonate to support optimal cell growth. Expression of hydroxymethyl glutaryl coenzyme A reductase mRNA was potently down-regulated by acLDL and exogenous desmosterol, but the effect was weaker with other sterol sources. We conclude that nLDL is more efficient than modified LDL in sustaining macrophage proliferation. Despite the requirement of cholesterol or desmosterol for J774 cell proliferation, excessive provision of either sterol limits mevalonate availability, thus suppressing cell proliferation. (C) 2008 Elsevier Inc. All rights reserved.
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