TY - JOUR
T1 - Effect of peroxisome proliferator-activated receptor gamma on thromboxane A2 and prostaglandin E2 production in macrophage cell lines
AU - Yamazaki, T.
AU - Yokoo, T.
AU - Tomioka, Y.
AU - Suzuki, H.
AU - Hishinuma, T.
AU - Mizugaki, M.
N1 - Funding Information:
A part of this study were supported by Grants-in-Aid for the Health Sciences Research Grants for the Research on Pharmaceutical and Medical Safety from the Ministry of Health and Welfare of Japan and the Research on Health Sciences Focusing on Drug Innovation from Japan Health Sciences Foundation.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 2002
Y1 - 2002
N2 - We studied the effect of peroxisome proliferator-activated receptor γ (PPARγ) activation on thromboxane A2(TXA2) and prostaglandin E2(PGE2) production in monocyte/macrophage cell lines. In present experiment, we used human peripheral blood monocyte (PBMC), monocyte-cell line THP-1 and mouse macrophage-like cell line RAW264.7. The expression of PPARγ is reported in PBMC and THP-1. Synthetic PPARγ ligands (troglitazone or BRL49653) inhibited TXA2 production and enhanced PGE2 production of PBMC and THP-1. When treated with 0.5-10 μM of troglitazone, there were no significant changes of TXA2 and PGE2 production of RAW264.7 cells, which express very low levels of PPARγ. When RAW264.7 cells was transfected with PPARγ expression plasmid and treated with troglitazone, PPARγ was activated in a dose-dependent manner. In PPARγ-transfected RAW264.7, TXA2 production was decreased and PGE2 production was increased by troglitazone treatment. But it needs high concentration of troglitazone (10 μM) for increasing PGE2 production. These results suggest that PPARγ may have negative effect on TXA2 production, and also have slightly positive effect on PGE2 production of macrophage.
AB - We studied the effect of peroxisome proliferator-activated receptor γ (PPARγ) activation on thromboxane A2(TXA2) and prostaglandin E2(PGE2) production in monocyte/macrophage cell lines. In present experiment, we used human peripheral blood monocyte (PBMC), monocyte-cell line THP-1 and mouse macrophage-like cell line RAW264.7. The expression of PPARγ is reported in PBMC and THP-1. Synthetic PPARγ ligands (troglitazone or BRL49653) inhibited TXA2 production and enhanced PGE2 production of PBMC and THP-1. When treated with 0.5-10 μM of troglitazone, there were no significant changes of TXA2 and PGE2 production of RAW264.7 cells, which express very low levels of PPARγ. When RAW264.7 cells was transfected with PPARγ expression plasmid and treated with troglitazone, PPARγ was activated in a dose-dependent manner. In PPARγ-transfected RAW264.7, TXA2 production was decreased and PGE2 production was increased by troglitazone treatment. But it needs high concentration of troglitazone (10 μM) for increasing PGE2 production. These results suggest that PPARγ may have negative effect on TXA2 production, and also have slightly positive effect on PGE2 production of macrophage.
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U2 - 10.1054/plef.2002.0426
DO - 10.1054/plef.2002.0426
M3 - Article
C2 - 12401439
AN - SCOPUS:0036797141
VL - 67
SP - 245
EP - 251
JO - Prostaglandins Leukotrienes and Essential Fatty Acids
JF - Prostaglandins Leukotrienes and Essential Fatty Acids
SN - 0952-3278
IS - 4
ER -