Philip Kingsley
Last active: 3/12/2020

RAW264.7 cells lack prostaglandin-dependent autoregulation of tumor necrosis factor-alpha secretion.

Rouzer CA, Jacobs AT, Nirodi CS, Kingsley PJ, Morrow JD, Marnett LJ
J Lipid Res. 2005 46 (5): 1027-37

PMID: 15722559 · DOI:10.1194/jlr.M500006-JLR200

Studies of the response of RAW264.7 cells (RAW) to lipopolysaccharide (LPS) were carried out to determine why these cells do not demonstrate the prostaglandin (PG)-dependent autocrine regulation of tumor necrosis factor-alpha (TNF-alpha) secretion observed in primary resident peritoneal macrophages (RPMs). The major cyclooxygenase (COX) product of LPS-stimulated RAW was PGD2, with lesser amounts of PGE2. LPS-treated RAW produced PGs more slowly and reached their maximal PG synthetic rate later than did LPS-treated RPMs, as a result of lower constitutive COX-1 expression and a slower rate of COX-2 induction. Cytosolic phospholipase A2 and levels of free arachidonic acid were similar in RAW and RPMs. In contrast to RPMs, LPS-treated RAW produced high quantities of TNF-alpha, which were not altered in the presence of COX inhibitors. This failure of endogenous PGs to suppress TNF-alpha secretion was explained by the absence of the prostaglandin D2 receptor and the low levels of PGE2 produced during the first 2 h of the LPS response. These studies demonstrate that autocrine regulation of TNF-alpha secretion in response to LPS is greatly facilitated by a COX-1-mediated rapid accumulation of PGs as well by a correspondence between the PGs produced and the receptors expressed by the cells.

MeSH Terms (10)

Animals Base Sequence Cell Line DNA Primers Lipopolysaccharides Macrophages Mice Prostaglandins Reverse Transcriptase Polymerase Chain Reaction Tumor Necrosis Factor-alpha

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