Disease relevance of Ptgds

• Lipocalin-type prostaglandin D2 synthase (L-PGDS) has recently been linked to a variety of pathophysiological cardiovascular conditions including hypertension and diabetes [1].
• Hypothyroidism alters the expression of prostaglandin D2 synthase/beta trace in specific areas of the developing rat brain [2].

High impact information on Ptgds

• Lipocalin-type prostaglandin D synthase (beta-trace) is located in pigment epithelial cells of rat retina and accumulates within interphotoreceptor matrix [3].
• The L-PGDS gene expression was up-regulated slowly by interleukin-1 beta to the maximum level at 24 h [4].
• Prostaglandin D2 synthase inhibits the exaggerated growth phenotype of spontaneously hypertensive rat vascular smooth muscle cells [1].
• Hematopoietic prostaglandin (PG) D synthase (PGDS) is the first identified vertebrate ortholog in the Sigma class of the glutathione S-transferase (GST) family and catalyzes both isomerization of PGH(2) to PGD(2) and conjugation of glutathione to 1-chloro-2, 4-dinitrobenzene [5].
• Lipocalin-type prostaglandin D synthase (beta-trace) is a newly recognized type of retinoid transporter [6].

Chemical compound and disease context of Ptgds

• These results show that hypothyroidism causes both age- and region-specific alterations in the expression and location of the prostaglandin D2 synthase during postnatal brain development, probably reflecting a cell-specific regulatory effect of thyroid hormone on the prostaglandin D2 synthase [2].

Biological context of Ptgds

• Identification of a thyroid hormone response element in the promoter region of the rat lipocalin-type prostaglandin D synthase (beta-trace) gene [7].
• Inhibition of cell cycle progression and migration of vascular smooth muscle cells by prostaglandin D2 synthase: resistance in diabetic Goto-Kakizaki rats [8].
• Prostaglandin D2 synthase induces apoptosis in PC12 neuronal cells [9].
• Secretion of lipocalin-type prostaglandin D synthase (beta-trace) from human heart to plasma during coronary circulation [10].

Anatomical context of Ptgds

• Lipocalin-type prostaglandin D synthase is responsible for the biosynthesis of prostaglandin D2 in the central nervous system and the genital organs and is secreted into the cerebrospinal fluid and the seminal plasma as beta-trace [6].
• Lipocalin-type prostaglandin D synthase is a major protein of the cerebrospinal fluid and was originally known as beta-trace [11].
• Localization of lipocalin-type prostaglandin D synthase (beta-trace) in iris, ciliary body, and eye fluids [12].
• Binding of biliverdin, bilirubin, and thyroid hormones to lipocalin-type prostaglandin D synthase [11].
• Cellular localization of lipocalin-type prostaglandin D synthase (beta-trace) in the central nervous system of the adult rat [13].

Associations of Ptgds with chemical compounds

• The localization of lipocalin-type prostaglandin D synthase in meningeal cells and its colocalization with COX-2 provide evidence for its function as a prostaglandin D(2)-producing enzyme [13].
• We analysed the effects of thyroid hormone deprivation on prostaglandin D2 synthase gene expression in the developing rat brain [2].
• In addition, prostaglandins E1, E2, and F2alpha all inhibited the PGD2S-induced apoptosis while prostaglandin H2 had no significant effect [9].
• Neutralization with anti-PGD2S antibody or pre-treatment with selenium, which inhibits PGD2S enzymatic activity, both significantly inhibited the PGD2S-induced apoptosis, however, neither had any effect on the apoptosis induced by the known neuronal apoptotic inducer, glutamate [9].
• It is in line with this observation that in vitro activation of protein kinase C of Kupffer cells resulted in a reduced PGE2 and an enhanced PGD2 synthase activity [14].

Analytical, diagnostic and therapeutic context of Ptgds

• Western blots with anti-lipocalin-type prostaglandin D synthase showed three distinct immunoreactive bands [3].
• By in situ hybridization, the strongest prostaglandin D2 synthase mRNA signal was detected in the leptomeninges and choroid plexus [2].

References