Disease relevance of Ptgfr

• Apoptosis and related proteins in placenta of intrauterine fetal death in prostaglandin f receptor-deficient mice [1].
• THG113: a novel selective FP antagonist that delays preterm labor [2].
• Both M-PGE and PGF resulted in a nearly 50% suppression of granuloma size following a 7-day course of treatment [3].
• In contrast, PGF did not ameliorate splenomegaly, but caused increases in splenic asialo-GM1 (natural killer cells) and L3T4 (helper) positive T cells [3].
• The decreased PGF and PGE2 production associated with this decreased bone resorption in the presence of non-toxic concentrations of indomethacin would suggest a role for these prostaglandins in maintaining the basal resorption of cultured bone [4].

High impact information on Ptgfr

• Prostanoids, including prostaglandin (PG) D(2), PGE(2), PGF(2alpha), PGI(2) and thromboxane (TX) A(2), exert their actions through specific receptors: DP, EP (EP(1), EP(2), EP(3), EP(4)), FP, IP and TP, respectively [5].
• The cytokine-induced increase in beating rate was markedly inhibited in atria from mice lacking either TP or FP receptors [5].
• Failure of parturition in mice lacking the prostaglandin F receptor [6].
• RNA blot and in situ hybridization analyses demonstrated that the PGF receptor transcripts are abundantly expressed in luteal cells of corpus luteum and in a lesser amount in kidney, heart, stomach, and lung [7].
• PGF2 alpha increased inositol trisphosphate formation in a concentration-dependent manner in COS cells expressing PGF receptor [7].

Chemical compound and disease context of Ptgfr

• Although PGF caused reduced granuloma macrophage Ia expression and O2- production, it did not suppress IL-1 production [3].
• Prostaglandin F2 alpha (PGF 2 alpha) has a bronchoconstrictive effect on the smooth muscles of the bronchial tree, while a prostaglandin of the E series (PGE) provokes bronchodilatation in bronchial asthma (BA) [8].

Biological context of Ptgfr

• Apoptosis and related proteins during parturition in prostaglandin F receptor-deficient mice [9].
• Female FP-/- mice are unable to deliver normal fetuses at term, as they do not undergo luteolysis necessary for parturition [10].
• In FP-expressing HEK293 cells, THG113 markedly reduced PGF2alpha-elicited phosphoinositide hydrolysis (IC50 27 nM) [2].
• Hormonal regulation of prostaglandin F2 alpha receptor gene expression in mouse ovary [11].
• Administration of pregnant mare serum gonadotropin (PMSG) to 35-day-old mice in the diestrus phase stimulated the ovary and enhanced the production of progesterone at 1 h PMSG also increased the ovarian PGF2 alpha receptor mRNA level in a time-dependent manner, reaching a sixfold maximum at 1 h [11].

Anatomical context of Ptgfr

• DNA laddering in the amnion, placenta and decidua tissue did not significantly differ between FP-deficient and wild type mice on day 18 of pregnancy [9].
• The index of TUNEL-positive cells were not significantly different in the amnion, placenta and decidua of FP-deficient mice compared with that of wild type mice on day 18 of pregnancy [9].
• In fura-2 fluorescence experiments, PGE2, sulprostone, PGF2alpha, fluprostenol (a potent FP agonist), and U-46619 (a selective thromboxane A2 agonist) induced a biphasic increase of [Ca2+]i in 60 to 80% of podocytes [12].
• Identification of a single (FP) receptor associated with prostanoid-induced Ca2+ signals in Swiss 3T3 cells [13].
• Abundant FP expression in ovarian follicles and uterus is consistent with previous reports of failed parturition in FP-/- mice [14].

Associations of Ptgfr with chemical compounds

• PGF2alpha receptor (FP) is coupled to stimulation of phospholipase C-inositol trisphosphate (IP3) pathway and Ca2+ mobilization [15].
• Sulprostone and (+)-fluprostenol failed to modulate any of responses tested, suggesting lack of involvement/expression of EP(1), EP(3), and FP receptors in DC activation [16].
• Control cultures prelabelled with either AA or EPA produced similar amounts of the respective PGF, PGE, and PGD [17].
• In the freeze-thawed preparations, use of AA as a substrate resulted in significantly more PGF than when EPA was used as the substrate [17].
• AL-3138 competed for [3H]PGF2alpha binding to FP receptors with a relatively high affinity (IC50high = 312 +/- 95 nM) matching its functional antagonist potency [18].

Regulatory relationships of Ptgfr

• These results strongly suggest that RA suppresses the phospholipase D activated by PGF2 alpha in osteoblast-like cells and that the effect of RA is exerted at the point between PGF2 alpha receptor and G-protein [19].

Other interactions of Ptgfr

• Ptgdr mapped to proximal Chr 14, Ptgfr mapped to distal Chr 3, Ptgerepl mapped to middle Chr 8, and Ptgir mapped to proximal Chr 7 [20].
• 3T3-L1 preadipocyte cells express mRNAs for the prostanoid EP4, FP, and IP receptors [21].
• Both in situ hybridization and beta-galactosidase knocked into the endogenous FP locus were used to determine the cellular distribution of the mouse FP receptor [14].
• Uterine expression of prostaglandin H2 synthase in late pregnancy and during parturition in prostaglandin F receptor-deficient mice [10].
• Role of prostaglandin H2 synthase 2 in murine parturition: study on ovariectomy-induced parturition in prostaglandin F receptor-deficient mice [22].

Analytical, diagnostic and therapeutic context of Ptgfr

• Similar TUNEL staining results were found in all tissues of FP-deficient mice compared with those of wild type mice [9].
• This study describes an effective and selective noncompetitive FP antagonist, THG113, which significantly delays preterm delivery; this provides the basis for future investigations for its use in tocolysis [2].
• Prostaglandin E (PGE) and prostaglandin F (PGF) levels, measured by radioimmunoassay, were much reduced in the EFA deficient mice skin [23].
• Northern blot analysis showed that the pattern of expression of the transgene corresponded to that of FP expression, except in the ovary [24].
• PGE and PGF were determined in endometrial curettage samples [25].

References