Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0184567 (
acute pain
)
3,962
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
PGs are potent mediators of pain and inflammation. PGE synthases (PGES) catalyze the isomerization of PGH(2) into PGE(2). The microsomal (m)
PGES-1
isoform serves as an inducible PGES and is responsible for the production of PGE(2), which mediates
acute pain
in inflammation and fever. The present study was designed to investigate the regulation of expression of
mPGES-1
in polarized phagocytes, which represent central, cellular orchestrators of inflammatory reactions. Here, we report that human peripheral blood monocytes did not express
mPGES-1
. Exposure to LPS strongly induced
mPGES-1
expression. Alternatively activated M2 monocytes-macrophages exposed to IL-4, IL-13, or IL-10 did not express
mPGES-1
, whereas in these cells, IL-4, IL-13, and to a lesser extent, IL-10 or IFN-gamma inhibited LPS-induced,
mPGES-1
expression. It is unexpected that polymorphonuclear leukocytes expressed high basal levels of
mPGES-1
, which was up-regulated by LPS and down-regulated by IL-4 and IL-13. Induction of
mPGES-1
and its modulation by cytokines were confirmed at the protein level and correlated with PGE(2) production. Cyclooxygenase 2 expression tested in the same experimental conditions was modulated in monocytes and granulocytes similarly to
mPGES-1
. Thus, activated M1, unlike alternatively activated M2, mononuclear phagocytes express
mPGES-1
, and IL-4, IL-13, and IL-10 tune expression of this key enzyme in prostanoid metabolism. Neutrophils, the first cells to enter sites of inflammation, represent a ready-made, cellular source of
mPGES-1
.
...
PMID:Regulation of the microsomal prostaglandin E synthase-1 in polarized mononuclear phagocytes and its constitutive expression in neutrophils. 1750 22
