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*
Harvard School of Public Health and
Harvard Medical School, Boston, MA 02115;
Lipid Metabolism Unit, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114
Gene deletion studies indicate that the macrophage scavenger
receptor A (SR-A) protects mice from LPS-induced endotoxemia.
Paradoxically, cultured human monocyte-derived macrophages
down-regulate SR-A expression when exposed to LPS. We found that human
THP-1 monocyte/macrophages decrease SR-A expression in response to LPS
independent of their differentiation status. In contrast, primary and
elicited mouse peritoneal macrophages as well as the J774A.1 and
RAW264.7 mouse macrophage lines increase SR-A expression in response to
LPS. Exposure to LPS caused J774A.1 and RAW264.7 cells to increase SR-A
transcripts by 3- and 5-fold, respectively. LPS caused a concomitant
3-fold increase in SR-A protein levels and increased cell membrane
expression of the receptor. RAW264.7 cells increased SR-A transcript
levels in response to LPS at concentrations as low as 1 ng/ml, and the
response was saturated at 10 ng/ml. The LPS induction of SR-A
transcripts required continual protein synthesis and began at 8 h,
peaked by 16 h, and persisted for at least 48 h. LPS
induction did not increase SR-A gene transcription or affect
alternative transcript splicing, but mildly increased mature transcript
stability and proceeded in the presence of actinomycin D. Finally,
treatment of RAW264.7 cells with TNF-
did not induce SR-A transcript
levels, indicating that a TNF- autocrine/paracrine signaling
mechanism alone is not sufficient to recapitulate the LPS induction of
SR-A transcripts. The induction of SR-A expression by LPS-stimulated
mouse macrophages is the opposite of the down-regulation of SR-A
reported in human monocyte-derived macrophages and may have
implications for the observed resistance mice show toward
endotoxemia.
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