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

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

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

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

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

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

17 L-PGDS overexpressing transgenic mice improved clearance o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

88 blot analysis using antisera to recombinant PGDS.

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

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

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