ライフサイエンスコーパス: PGDS

1 PGDS isolated from corneal extracts was not keratanase s

2 epididymal expression possibly appeared in a PGDS-like lipocalin in amniotes, and the duplications ge

3 rance and returned the synthesis of decorin, PGDS, and keratan sulfate to keratocyte levels.

4 ted that selenoproteins were necessary for H-PGDS expression and 15d-PGJ(2) production.

5 uggesting a positive feedback mechanism of H-PGDS expression.

6 e expression of COX-1, hematopoietic-PGDS (H-PGDS), cytosolic-PGES (c-PGES), or mPGES-2 in BMDM was n

7 howed that coincubation of the recombinant H-PGDS with either MnTMPyP, EUK-134, or catalase significa

8 ivated receptor gamma ligand, up-regulated H-PGDS.

9 pression of hematopoietic-PGD(2) synthase (H-PGDS) by selenium and a corresponding increase in Delta(

10 ound that both hematopoietic PGD synthase (H-PGDS) siRNA and its inhibitor HQL-79, but not lipocalin

11 ression of hematopoietic- PGD(2) synthase (H-PGDS) to effect endogenous production of CyPGs, through

12 induced PGD(2) production, suggesting that H-PGDS, but not L-PGDS, mediates LPS-induced PGD(2) produc

13 ferentially and specifically regulates the H-PGDS-mediated production of PGD(2), but not PGE(2), in m

14 rast, the expression of COX-1, hematopoietic-PGDS (H-PGDS), cytosolic-PGES (c-PGES), or mPGES-2 in BM

15 s of meningioma - Pik3ca or AKT1 (E17K) - in PGDS-positive cells, a spectrum of typical CCMs develops

16 L-PGDS (50 microg/ml) was able to significantly inhibit VS

17 L-PGDS expression also increased 50% upon the differentiat

18 L-PGDS expression was detected in whole lung and alveolar

19 l-PGDS interacted preferentially with the inactive, GDP-lo

20 L-PGDS overexpressing transgenic mice improved clearance o

21 L-PGDS promotes cell surface expression of DP1, but not of

22 l-PGDS/Rab4 and DP1/Rab4 co-immunoprecipitation levels wer

23 caveolin-1 expression by > 2.5-fold in an L-PGDS-dependent manner.

24 marked rise in COX (cyclooxygenase)-2 and L-PGDS (lipocalin-type prostaglandin D synthase) expressio

25 nted l-PGDS-mediated recycling of DP1, and l-PGDS depletion inhibited Rab4-dependent recycling of DP1

26 ucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 leve

27 of microsomal PGE synthase-1 (mPGES-1) and L-PGDS.

28 ce is dependent on the interaction between L-PGDS and the C-terminal MEEVD residues of Hsp90.

29 Surprisingly, PGD2 synthesis by L-PGDS is promoted by coexpression of DP1, suggesting a po

30 ated ERK phosphorylation was unaffected by L-PGDS pretreatment in both cell lines.

31 terminus with Rab4, which was increased by l-PGDS.

32 Enzymatic products of stromal cell L-PGDS included high levels of PGD2 and 15-deoxy-delta(12,

33 abolished by AT-56, a specific competitive L-PGDS inhibitor.

34 In contrast, L-PGDS knockout mice were impaired in their ability to rem

35 ating for a lack of PPARgamma2, we crossed L-PGDS KO mice to PPARgamma2 KO mice to generate Double Kn

36 ncentrations (20 mm) resulted in decreased L-PGDS expression in control cells but actually stimulated

37 (DP1) promotes the activity of the enzyme (L-PGDS) that produces its agonist (PGD2) and in which this

38 Pulldown assays with purified GST-l-PGDS and His(6)-Rab4 indicated that both proteins intera

39 Our results reveal how l-PGDS, which produces the agonist for DP1, regulates DP1

40 eptides revealed that amino acids 85-92 in l-PGDS are involved in its interaction with Rab4 and in it

41 dization revealed significant increases in L-PGDS expression in the arcuate and ventromedial nucleus

42 focal adhesion kinase expression levels in L-PGDS KO vascular smooth muscle cells and controls.

43 is study, we report on the 50% increase in L-PGDS protein expression observed in vascular smooth musc

44 ial endotoxin (LPS) or Pseudomonas induced L-PGDS expression.

45 scopy revealed that DP1 activation induces l-PGDS/Rab4 co-localization.

46 r cold-acclimated conditions, mice lacking L-PGDS had elevated reliance on carbohydrate to provide fu

47 ncreases glucose utilization, mice lacking L-PGDS had improved glucose tolerance after high-fat feedi

48 Moreover, L-PGDS knockout mice exhibited increased expression of gen

49 roduction, suggesting that H-PGDS, but not L-PGDS, mediates LPS-induced PGD(2) production in BMDM.

50 , in HEK293 and HeLa cells, independent of L-PGDS enzyme activity.

51 ogether, our results identify induction of L-PGDS expression by inflammatory stimuli or bacterial inf

52 PGDS induction, and the protective role of L-PGDS expression in host immune response.

53 owever, the regulation and significance of L-PGDS expression in macrophages are unknown.

54 Epigenetic suppression of L-PGDS expression in macrophages blunted a majority of PGD

55 DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) functio

56 Consistent with the concept that lack of L-PGDS increases glucose utilization, mice lacking L-PGDS

57 Furthermore, we examined the effect of L-PGDS incubation on insulin-stimulated Akt, glycogen synt

58 ial infection, the regulatory mechanism of L-PGDS induction, and the protective role of L-PGDS expres

59 suggests a potential therapeutic usage of L-PGDS or PGD(2) against Pseudomonas pneumonia.

60 iguing possibility that E(2) modulation of L-PGDS plays a role in the regulation of sleep-wake states

61 Catalytic activity of L-PGDS produces PGD2, an endogenous somnogen.

62 As predicted from E2 suppression of L-PGDS transcript levels, the responses of the locked nucl

63 on, we demonstrate differential effects of L-PGDS treatment on cell proliferation and apoptosis in VS

64 To determine if induction of L-PGDS was compensating for a lack of PPARgamma2, we cross

65 Overall, L-PGDS and PPARgamma2 coordinate to regulate carbohydrate

66 inhibitor HQL-79, but not lipocalin PGDS (L-PGDS) siRNA and its inhibitor AT-56, significantly atten

67 Depletion of endogenous Rab4 prevented l-PGDS-mediated recycling of DP1, and l-PGDS depletion inh

68 Thus, reducing L-PGDS in the VLPO of oil-treated females mimicked the eff

69 In this regard, L-PGDS increases the formation of a DP1-ERK1/2 complex and

70 -fibroblast adhesion, IL-33-ST2 signaling, L-PGDS-driven PGD(2) generation, and feedforward ATX-LPA(1

71 n in control cells but actually stimulated L-PGDS expression in SHR.

72 Surprisingly, L-PGDS gene expression is reduced 2-fold after E(2) treatm

73 t lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D2 (PGD2) metabolites produced b

74 , Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyzed

75 els of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose t

76 Lipocalin-type prostaglandin D2 synthase (L-PGDS) has recently been linked to a variety of pathophys

77 ndogenous L-type prostaglandin D synthase (L-PGDS) in HeLa cells inhibited recycling of the prostagla

78 le for lipocalin prostaglandin D synthase (L-PGDS) in the control of metabolic fuel utilization by br

79 lin-type prostaglandin D2 (PGD2) synthase (L-PGDS) interacts intracellularly with the GPCR DP1 in an

80 uronal cells, lipocalin-type PGD synthase (L-PGDS) is detected in the macrophages infiltrated to athe

81 n lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, after E2 treatment, in the vent

82 ipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at elevated levels in type 2 diab

83 s lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycoprotein (AAG), transferrin (T

84 is lipocalin prostaglandin D(2) synthase (L-PGDS), which catalyzes the conversion of prostaglandin (

85 , the prostaglandin D(2) (PGD(2)) synthase L-PGDS, or the PGD(2) receptor DP1, impairs MC maturation

86 says with purified proteins suggested that l-PGDS enhances GDP-GTP exchange on Rab4.

87 We demonstrate that L-PGDS expression in BAT is positively correlated with BAT

88 matin immunoprecipitation assays show that L-PGDS induction was regulated positively by AP-1, but neg

89 we demonstrate, immunocytochemically, that L-PGDS is also expressed in a population of VLPO neurons.

90 We propose that L-PGDS is involved in the balance of VSMC proliferation an

91 Our results show that L-PGDS KO mice become glucose-in-tolerant and insulin-resi

92 r agonist-induced internalization and that L-PGDS overexpression had the opposite effect.

93 n and depletion experiments disclosed that l-PGDS partakes in Rab4 activation following DP1 stimulati

94 Taken together, these results suggest that L-PGDS plays an important role in the regulation of glucos

95 We conclude that L-PGDS plays an important role regulating insulin sensitiv

96 Immunostaining showed that L-PGDS was expressed in the neurons of human myenteric and

97 dipocytes were significantly larger in the L-PGDS KO mice compared with controls on the same diets.

98 In addition, only the L-PGDS KO mice developed nephropathy and an aortic thicken

99 and elevated serum FFA levels compared to L-PGDS KO alone.

100 ties (an improved technology), targeted to L-PGDS mRNA, (ii) scrambled sequence control oligos, or (i

101 Finally, whereas L-PGDS has been reported to be expressed primarily in olig

102 d that when WKY cells were pretreated with L-PGDS, insulin could actually induce apoptosis and failed

103 and its inhibitor HQL-79, but not lipocalin PGDS (L-PGDS) siRNA and its inhibitor AT-56, significant

104 The accumulation of PGDS, a KSPG that does not interact with collagen, was n

105 Additionally, these cells produce PGDS, a known retinoid transporter, as a KSPG.

106 blot analysis using antisera to recombinant PGDS.

107 ly lower levels of prostaglandin D synthase (PGDS) and keratan sulfate.

108 at the protein was prostaglandin D synthase (PGDS).

109 th the use of the prostaglandin D2 synthase (PGDS) promoter.

110 ses, PGE synthases (PGES) and PGD synthases (PGDS), respectively.

111 a and AKT1 (E17K) in mice and identified the PGDS-expressing pericyte as the probable cell of origin.