2‐Cyclopenten‐1‐one and prostaglandin J2 reduce restenosis after balloon angioplasty in rats: role of NF‐κB

• Published in: FEBS letters Vol. 553; no. 1-2; pp. 21 - 27
• Main Authors: Ianaro, Angela, Maffia, Pasquale, Cuzzocrea, Salvatore, Mazzon, Elena, Santoro, Maria Gabriella, Di Rosa, Massimo, Ialenti, Armando
• Format: Journal Article
• Language: English
• Published: 09.10.2003
• Subjects: 2-Cyclopenten-1-one; Cyclopentenone prostaglandin; cyPG, cyclopentenone prostaglandin; EMSA, electrophoretic mobility shift assay; ICAM-1, intercellular adhesion molecule-1; IEL, internal elastic lamina; IKK, I-κB kinase; L-PDGS, lipocalin-type prostaglandin D synthase; NF-κB, nuclear factor-κB; Nuclear factor-κB; PPARγ, peroxisome proliferator-activated receptor-γ; PTCA, percutaneous transluminal coronary angioplasty; Restenosis; VSMC, vascular smooth muscle cell
• ISSN: 0014-5793; 1873-3468
• DOI: 10.1016/S0014-5793(03)00873-1

The aim of this study was to evaluate, using a rat model of balloon angioplasty, whether prostaglandin (PG) J2 and 2‐cyclopenten‐1‐one are able to reduce restenosis. We found that both PGJ2 and 2‐cyclopenten‐1‐one, administered by local application on carotid arteries, caused a dose‐dependent inhibition of neointimal formation. Furthermore, both agents prevented vascular negative remodeling. The effect of these compounds on restenosis was correlated with an inhibition of nuclear factor‐κB (NF‐κB) activation as well as of intercellular adhesion molecule‐1 (ICAM‐1) protein expression in injured carotid arteries of control animals. Our results show that cyclopentenone PGs and their derivatives reduce restenosis and may have therapeutic relevance for the prevention of human restenosis.