ライフサイエンスコーパス: prostaglandin D

1 polipoprotein E, protein phosphatase 2A, and prostaglandin D.

2 ve agonist of the DP(2) receptor, 15R-methyl prostaglandin D(2) (15R-D(2)).

3 stingly, IL-4 increases endogenous levels of prostaglandin D(2) (PGD(2) ) and its metabolites, Delta(

4 Current research suggests that the prostaglandin D(2) (PGD(2) ) receptor 2 (DP(2) ) is a pr

5 tamine, cysteinyl-leukotrienes (cys-LTs) and prostaglandin D(2) (PGD(2) ) was assessed as was express

6 uld involve type 2 cytokines (IL5, IL13) and prostaglandin D(2) (PGD(2) ).

7 to biosynthesize lipid mediators other than prostaglandin D(2) (PGD(2)) and the cysteinyl leukotrien

8 DS) in HeLa cells inhibited recycling of the prostaglandin D(2) (PGD(2)) DP1 receptor (DP1) to the ce

9 Here, we show that increases in prostaglandin D(2) (PGD(2)) expression in mouse lungs up

10 hat mediates the pro-inflammatory effects of prostaglandin D(2) (PGD(2)) generated in allergic inflam

11 or upregulating COX-2 expression and causing prostaglandin D(2) (PGD(2)) generation.

12 lt of increased levels of the lipid mediator prostaglandin D(2) (PGD(2)) in the respiratory tract wit

13 Prostaglandin D(2) (PGD(2)) is a cyclooxygenase (COX) pr

14 Prostaglandin D(2) (PGD(2)) is known to have antipruriti

15 omologous molecule on Th2 cells (CRTH2) is a prostaglandin D(2) (PGD(2)) receptor, expressed by Th2 c

16 Prostaglandin D(2) (PGD(2)) signals through the G protei

17 , like that of the phospholipase PLA2G3, the prostaglandin D(2) (PGD(2)) synthase L-PGDS, or the PGD(

18 dependent, elevated levels of an eicosanoid (prostaglandin D(2) (PGD(2))) and a phospholipase (phosph

19 o mediate the metabolism of sex hormones and prostaglandin D(2) (PGD(2)), a lipid mediator that promo

20 pressed on TH2 cells (CRTH2), a receptor for prostaglandin D(2) (PGD(2)), is expressed by human ILC2s

21 nism, thought to be caused by the release of prostaglandin D(2) (PGD(2)), is not well understood.

22 Prostaglandin D(2) (PGD(2)), mainly produced by mast cel

23 e effect of inhaled PGE(2) on the release of prostaglandin D(2) (PGD(2)), preformed mast cell mediato

24 (CRTH2), a receptor for the bioactive lipid prostaglandin D(2) (PGD(2)).

25 racerebroventricular (icv) administration of prostaglandin D(2) (PGD(2); 20 microg/5 microl) to consc

26 Prostaglandin D(2) (PGD2), which reduces DC migration th

27 Prostaglandin D(2) and CXCL12 levels in BAL fluid correl

28 while triggering prostanoid (thromboxane and prostaglandin D(2) and E(2) ) production.

29 Prostaglandin D(2) and its cyclopentenone metabolites [c

30 Serum prostaglandin D(2) and leukotriene E(4) levels were sign

31 olizumab, as were urinary levels of tetranor-prostaglandin D(2) and leukotriene E(4).

32 es, eosinophils and basophils in response to prostaglandin D(2) and may be involved in the pathogenes

33 Urinary prostaglandin D(2) and thromboxane metabolites decreased

34 ts as specific therapies for this condition (prostaglandin D(2) antagonists or cytokine antagonists [

35 obese human arteries with FTO inhibitors or prostaglandin D(2) application.

36 activation of Crth2 by 13,14-dihydro-15-keto-prostaglandin D(2) increased Ca(2+) influx through store

37 tion of L-Pgds with significant increases in prostaglandin D(2) levels.

38 In the developing testis, prostaglandin D(2) may act as a paracrine factor to indu

39 nthesis of the clinically relevant tricyclic prostaglandin D(2) metabolite (tricyclic-PGDM) methyl es

40 or increases in urinary leukotriene E(4) and prostaglandin D(2) metabolite levels during aspirin-indu

41 lated with peak urinary leukotriene E(4) and prostaglandin D(2) metabolite levels in participants tak

42 nd aspirin-induced urinary leukotriene E(4), prostaglandin D(2) metabolite, and serum tryptase levels

43 duced increases in urinary leukotriene E(4), prostaglandin D(2) metabolite, or thromboxane B(2) level

44 Nasal prostaglandin F(2a), prostaglandin D(2) metabolites, leukotriene B(4), and th

45 had a tendency to release more tryptase and prostaglandin D(2) on anti-IgE stimulation of bronchoalv

46 mRNA expression of PLA(2)G2D and prostaglandin D(2) receptor (PTGDR), and production of P

47 to determine the efficacy and safety of the prostaglandin D(2) receptor 2 (DP(2)) antagonist fevipip

48 population displaying markers of both ILC2s (prostaglandin D(2) receptor 2; CRTH2, IL-5, and IL-13) a

49 thesis was developed for the production of a prostaglandin D(2) receptor antagonist for the treatment

50 for the production of the core structure of prostaglandin D(2) receptor antagonists for the treatmen

51 ene receptors antagonists, and more recently prostaglandin D(2) receptor antagonists, have been shown

52 Here, we show that rodent GnRH neurons use a prostaglandin D(2) receptor DP1 signaling mechanism duri

53 tment of bone marrow-derived mast cells with prostaglandin D(2) reduced their ability to generate leu

54 ed by CD34(+) cells, decreased apoptosis and prostaglandin D(2) release by cultured MCs, and higher p

55 igh-fat diet; conversely, direct addition of prostaglandin D(2) rescued myogenic tone in high-fat die

56 ot, confocal microscopy, cell degranulation, prostaglandin D(2) secretion, and proteases gene transcr

57 /2 inhibitor flurbiprofen, the hematopoietic prostaglandin D(2) synthase (HPGDS) inhibitor KMN698, an

58 cts of gene knock-out (KO) of lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at

59 Most striking is lipocalin prostaglandin D(2) synthase (L-PGDS), which catalyzes th

60 al literature identifies a sex difference in prostaglandin D(2) synthase (PTGDS) expression where it

61 transcript 6), and a prostaglandin synthase (prostaglandin D(2) synthase).

62 Blockade of prostaglandin D(2) synthesis inhibited the myogenic tone

63 J(2)) are naturally occurring derivatives of prostaglandin D(2) that have been suggested to exert ant

64 sease severity; urinary leukotriene E(4) and prostaglandin D(2) were quantified in a subgroup (n = 72

65 Bronchoalveolar lavage (BAL) fluid prostaglandin D(2)(PGD(2)) levels are increased in patie

66 allergy (such as cysteinyl leukotrienes and prostaglandin D(2)) and the neurotransmitter acetylcholi

67 d an increased anti-inflammatory derivative (prostaglandin D(2)).

68 mediators from mast cells such as histamine, prostaglandin D(2), and cysteinyl leukotrienes.

69 with high levels of cysteinyl leukotrienes, prostaglandin D(2), and low levels of prostaglandin E(2)

70 ew blockers of specific mediators, including prostaglandin D(2), IL-5, IL-9, and IL-13, are also in c

71 Exocytosis and the generation of prostaglandin D(2), LTB(4), and 5-hydroxyeicosatetraenoi

72 ells stimulated the synthesis and release of prostaglandin D(2), to our knowledge a previously unrepo

73 blasts, or by intraepithelial events such as prostaglandin D(2)-dependent reduced HF epithelial stem

74 ls, eosinophils and basophils in response to prostaglandin D(2).

75 s masculinising environment is to synthesise prostaglandin D(2).

76 onic acid-derived signaling entities such as prostaglandin D(2).

77 ry (LC-MS/MS) assay that accurately measures prostaglandins D(2) (PGD(2)) and E(2) (PGE(2)) in cell c

78 increases in other COX metabolites including prostaglandins D(2) , F(2a) , and I(2) .

79 ts of PGD(2), prostaglandin J(2), as well as prostaglandin D receptor (DP) agonists and antagonists o

80 ing, chemokine ligand 5 (CCL5) hematopoietic prostaglandin D synthase (HPGDS) and neuropeptide S rece

81 PGD(2), which is generated by hematopoietic prostaglandin D synthase (HPGDS), acts on 3 G protein-co

82 Our results show that lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D2 (

83 n proinflammatory conditions, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons

84 e found to have elevated levels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and

85 e report that depletion of endogenous L-type prostaglandin D synthase (L-PGDS) in HeLa cells inhibite

86 is study, we define a new role for lipocalin prostaglandin D synthase (L-PGDS) in the control of meta

87 trated a twofold reduction in lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, aft

88 ed for the urinary biomarkers lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycop

89 of decorin and significantly lower levels of prostaglandin D synthase (PGDS) and keratan sulfate.

90 cid sequencing revealed that the protein was prostaglandin D synthase (PGDS).

91 ression of prostaglandin synthase-1 (PGHS1), prostaglandin D synthase (PTGDS), human prostaglandin tr

92 Prostaglandin D synthase and tryptase transcripts were e

93 cological blockade of cyclooxygenase-2 or of prostaglandin D synthase prevented the effects of increa

94 ient substrate for the hematopoietic type of prostaglandin D synthase resulting in formation of HKD(2

95 cyclooxygenase)-2 and L-PGDS (lipocalin-type prostaglandin D synthase) expression, which appeared to

96 Sigma class GST (Prostaglandin D synthase), FhGST-S1, is present in the e

97 ilar to those of GSH-dependent hematopoietic prostaglandin D synthase, except for the two large loop

98 ssociated with allergic responses, including prostaglandin D synthase, histamine receptor type 1 (H1R

99 ich inhibit cyclooxygenases or hematopoietic prostaglandin D synthase, respectively, or use of Crth2

100 reater IL-5 and IL-13 than did hematopoietic prostaglandin D synthase-negative and CD161(-) cT(H)2 ce

101 H)2 cells-positive (CRTH2(+)), hematopoietic prostaglandin D synthase-positive CD161(hi) CD4 T cells.