Disease relevance of prostaglandin J2

• We hypothesize that an altered expression of enzymes in PGJ2 synthesis may represent a novel pathogenic mechanism in human obesity [1].
• By contrast, the modulation of differentiation-associated proteins by PGJ2, but not rosiglitazone, suggests that PGJ2 promotes differentiation of glioblastoma cells independently of PPARgamma activation [2].
• Among PPARgamma ligands, 15-deoxy-Delta12,14-prostaglandin J2 (PGJ2), the ultimate metabolite of PGD2, plays a role in the biology of brain tumors [2].
• The effects of PGD2 and 9-deoxy-delta 9-PGD2 on colony formation of murine osteosarcoma cells [3].
• Ciglitazone and PGJ2 inhibited melanoma cell proliferation in a dose-dependent manner [4].

High impact information on prostaglandin J2

• Based on the 50% inhibitory dose, PGJ2 and its analogues were from two to five times more potent than PGA1 [5].
• Furthermore, neither 15d-PGJ2 nor PGJ2 were able to induce expression of the UPII gene in NHU cells, in contrast to cultures exposed to the pharmacologic PPAR-gamma agonist, troglitazone [6].
• Prostaglandin J2 (PGJ2) and delta12-PGJ2, AA metabolites formed in the COX pathway, induced K2 cell death [7].
• Both ciglitazone and PGJ2 increased baseline synaptic transmission significantly, without altering paired-pulse facilitation [8].
• Pretreatment of RINm5F cells for 6 h with PGJ2 results in inhibition of IL-1-stimulated IkappaB degradation and IFN-gamma-stimulated STAT1 phosphorylation [9].

Biological context of prostaglandin J2

• Although these agents fail to attenuate the inhibitory actions of PGJ2 on cytokine signaling, they do inhibit PGJ2-stimulated PPARgamma response element reporter activity [9].
• M059K cells committed to undergo apoptosis by PGJ2, initially up-regulated PPARgamma, and then down-regulated PPARgamma as they began apoptosis [2].
• A dose-dependent inhibition of TA 102 colony formation was also observed with 9-deoxy-delta 9-PGD2 between 0.01 to 1 microgram/ml, the IC50 value being 0.22 microgram/ml [3].
• Induction of PPARgamma-dependent transactivation by 15-deoxy-Delta12,14-prostaglandin J2 (PGJ2) and DIM-C-pPhCF(3) was inhibited in MCF-7 cells cotreated with the PPARgamma-specific antagonist N-(4'-aminopyridyl)-2-chloro-5-nitrobenzamide [10].

Anatomical context of prostaglandin J2

• To determine the impact of PPARgamma on steroidogenesis, granulosa cells were collected from ovaries 24 h post-eCG and cultured alone, with FSH alone, or with FSH in combination with the PPARgamma agonists ciglitazone or 15-deoxy-delta 12,14-prostaglandin J2 (PGJ2) [11].
• Our data indicate that PGJ2, and rosiglitazone suppress cell proliferation and cause apoptosis in glioblastoma cell lines, most likely through a PPARgamma-dependent pathway [2].
• Modulation of lymphocyte and monocyte responses in vitro by 9-deoxy-delta 9-prostaglandin D2 and 9-deoxy-delta 9-delta 12-prostaglandin D2 [12].

Associations of prostaglandin J2 with other chemical compounds

• Treatment of granulosa cells with PGJ2 stimulated basal progesterone secretion, whereas ciglitazone or PGJ2 had no significant effect on FSH-stimulated steroid production [11].
• Prostaglandin D2 spontaneously decomposes at physiological pH and temperature to 9-deoxy-delta 9-PGD2 (designated PGJ2) [13].

Gene context of prostaglandin J2

• Unexpectedly, PGJ2 up-regulated the expression of cyclooxygenase-2 (COX-2) [2].
• PGJ2 increased expression of glial fibrillary acidic protein (GFAP) and decreased levels of vimentin, structural proteins modulated during astrocytic differentiation [2].

References