15-Deoxy-Δ12,14-prostaglandin J2 induces PPARγ- and p53-independent apoptosis in rabbit synovial cells.

A ligand of peroxisome proliferator-activated receptor γ (PPARγ), 15-deoxy-Δ(12,14)-prostaglandin J2 (15d-PGJ2) induces apoptosis in various cells. However, the mechanism appears to be complex and cell-type specific. We investigated the mechanism of 15d-PGJ2-induced apoptosis of rabbit synovial cells.

Mechanical stretch enhances NF-kappaB-dependent gene expression and poly(ADP-ribose) synthesis in synovial cells.

Temporomandibular joint disorders (TMD) show complex symptoms associated with inflammation, pain and degeneration of the peripheral tissues including synovium. Although it is believed that excessive mechanical stress on synovium causes development of TMD, the molecular mechanism by which mechanical stress triggers TMD has still remained unclear. In order to examine the effect of mechanical stress on synoviocytes, rabbit synovial cells were cyclically stretched in vitro.

15-Deoxy-Delta(12,14)-prostaglandin J(2) impairs the functions of histone acetyltransferases through their insolubilization in cells.

The cyclopentenonic prostaglandin 15-deoxy-Delta(12,14)-PG J(2) (15d-PGJ(2)) is a metabolite derived from PGD(2). Although 15d-PGJ(2) has been demonstrated to be a potent ligand for peroxisome proliferator activated receptor gamma (PPARgamma), the functions are not fully understood. In order to examine the effect of 15d-PGJ(2) on histone acetyltransferases (HATs), several lines of cell including mouse embryonic fibroblast (MEF) cells were exposed to 15d-PGJ(2).