Role of PPAR-beta in hydrogen peroxide-induced apoptosis in human umbilical vein endothelial cells.

Abstract

Peroxisome proliferator-activated receptor beta (PPAR-beta) is a ligand activated transcription factor belonging to the nuclear receptor superfamily. Recent evidence suggests that PPAR-beta has clearly defined roles in skin wound healing, inflammation and cell proliferation. However, little is known about the role of PPAR-beta in oxidative stress-induced apoptosis in human umbilical vein endothelial cells (HUVECs). In this study, a specific PPAR-beta ligand, L-165041, and antisense phosphorothioate oligodeoxynucleotides (asODNs) against PPAR-beta were used to reveal the role of PPAR-beta in oxidative stress-induced apoptosis. The results showed that H(2)O(2) at 0.5mM resulted in a marked increase of apoptosis and a significant down-regulation of PPAR-beta expression and activation in HUVECs. Moreover, L-165041 significantly inhibited H(2)O(2)-induced apoptosis (P<0.05) and asODNs against PPAR-beta markedly inhibited the de novo synthesis of PPAR-beta, which was accompanied by enhanced apoptosis induced by H(2)O(2) (P<0.05). These data demonstrated that H(2)O(2) down-regulated the expression and activation of PPAR-beta, which played important roles in H(2)O(2)-induced apoptosis in HUVECs.

• Authors: Bimei Jiang, Pengfei Liang, Bing Zhang, Juan Song, Xiaoyuan Huang, Xianzhong Xiao
• Journal: Atherosclerosis (Atherosclerosis) Vol. 204 Issue 2 Pg. 353-8 (Jun 2009) ISSN: 1879-1484 [Electronic] Ireland
• PMID: 18937948 (Publication Type: Journal Article)

Chemical References

• 4-(3-(2-propyl-3-hydroxy-4-acetyl)phenoxy)propyloxyphenoxy acetic acid
• Oligodeoxyribonucleotides, Antisense
• Oxidants
• PPAR-beta
• Phenoxyacetates
• Phosphorothioate Oligonucleotides
• DNA
• Hydrogen Peroxide

Topics

• Apoptosis (drug effects)
• Binding Sites
• Cells, Cultured
• DNA (metabolism)
• Dose-Response Relationship, Drug
• Endothelial Cells (drug effects, metabolism, pathology)
• Humans
• Hydrogen Peroxide (toxicity)
• Oligodeoxyribonucleotides, Antisense (metabolism)
• Oxidants (toxicity)
• PPAR-beta (agonists, genetics, metabolism)
• Phenoxyacetates (pharmacology)
• Phosphorothioate Oligonucleotides (metabolism)
• Time Factors
• Transcription, Genetic (drug effects)
• Umbilical Veins (drug effects, metabolism, pathology)