15-Deoxy-prostaglandin J2 inhibits PDGF-A and-B chain expression in human vascular endothelial cells independent of PPARγ

J Zhang, M Fu, L Zhao, YE Chen - Biochemical and biophysical research …, 2002 - Elsevier
J Zhang, M Fu, L Zhao, YE Chen
Biochemical and biophysical research communications, 2002Elsevier
15-Deoxy-prostaglandin J 2 (15 d-PGJ 2) is an endogenous ligand of peroxisome
proliferator-activated receptor γ (PPARγ) and plays an important role in the regulation of
endothelial cell growth and apoptosis. However, the detailed mechanisms are poorly
understood. We hypothesized that 15d-PGJ2 might affect PDGF expression in endothelial
cells through activating PPARγ. Here we documented that 15d-PGJ2 dose-dependently
inhibited phorbol-12-myristate-13-acetate (PMA)-stimulated expression of the PDGF-A and …
15-Deoxy-prostaglandin J 2(15 d-PGJ 2) is an endogenous ligand of peroxisome proliferator-activated receptor γ (PPARγ) and plays an important role in the regulation of endothelial cell growth and apoptosis. However, the detailed mechanisms are poorly understood. We hypothesized that 15d-PGJ2 might affect PDGF expression in endothelial cells through activating PPARγ. Here we documented that 15d-PGJ2 dose-dependently inhibited phorbol-12-myristate-13-acetate (PMA)-stimulated expression of the PDGF-A and PDGF-B chain in human umbilical vein endothelial cells (HUVEC) by Northern blot and Western blot analyses. In contrast, the synthetic and high-affinity PPARγ agonists, including ciglitazone and GW7845, did not affect PMA-induced PDGF expression. In addition, we found that the PPARγ antagonist GW9662 did not block the effects of 15d-PGJ2 on PDGF expression. Furthermore, Northern blot analysis showed that 15d-PGJ2 inhibited the expression of Sp1, which is a well-known positive regulator of PDGF transcription. Taken together, our results demonstrate that the inhibition of PDGF expression by 15d-PGJ2 in HUVEC is independent of PPARγ, but may be through the downregulation of Sp1.
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