ライフサイエンスコーパス: L-PGDS

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

2 L-PGDS expression also increased 50% upon the differenti

3 L-PGDS expression was detected in whole lung and alveola

4 L-PGDS overexpressing transgenic mice improved clearance

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

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

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

8 a marked rise in COX (cyclooxygenase)-2 and L-PGDS (lipocalin-type prostaglandin D synthase) express

9 mucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 le

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

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

12 ulated ERK phosphorylation was unaffected by L-PGDS pretreatment in both cell lines.

13 Enzymatic products of stromal cell L-PGDS included high levels of PGD2 and 15-deoxy-delta(1

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

15 In contrast, L-PGDS knockout mice were impaired in their ability to r

16 nsating for a lack of PPARgamma2, we crossed L-PGDS KO mice to PPARgamma2 KO mice to generate Double

17 concentrations (20 mm) resulted in decreased L-PGDS expression in control cells but actually stimulat

18 R (DP1) promotes the activity of the enzyme (L-PGDS) that produces its agonist (PGD2) and in which th

19 this study, we report on the 50% increase in L-PGDS protein expression observed in vascular smooth mu

20 ridization revealed significant increases in L-PGDS expression in the arcuate and ventromedial nucleu

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

22 erial endotoxin (LPS) or Pseudomonas induced L-PGDS expression.

23 der cold-acclimated conditions, mice lacking L-PGDS had elevated reliance on carbohydrate to provide

24 increases glucose utilization, mice lacking L-PGDS had improved glucose tolerance after high-fat fee

25 Moreover, L-PGDS knockout mice exhibited increased expression of g

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

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

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

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

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

31 Together, our results identify induction of L-PGDS expression by inflammatory stimuli or bacterial i

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

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

34 erial infection, the regulatory mechanism of L-PGDS induction, and the protective role of L-PGDS expr

35 triguing possibility that E(2) modulation of L-PGDS plays a role in the regulation of sleep-wake stat

36 ng DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) funct

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

38 However, the regulation and significance of L-PGDS expression in macrophages are unknown.

39 Epigenetic suppression of L-PGDS expression in macrophages blunted a majority of P

40 As predicted from E2 suppression of L-PGDS transcript levels, the responses of the locked nu

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

42 Overall, L-PGDS and PPARgamma2 coordinate to regulate carbohydrat

43 ts inhibitor HQL-79, but not lipocalin PGDS (L-PGDS) siRNA and its inhibitor AT-56, significantly att

44 Thus, reducing L-PGDS in the VLPO of oil-treated females mimicked the e

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

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

47 ion in control cells but actually stimulated L-PGDS expression in SHR.

48 Surprisingly, L-PGDS gene expression is reduced 2-fold after E(2) trea

49 G3, the prostaglandin D(2) (PGD(2)) synthase L-PGDS, or the PGD(2) receptor DP1, impairs MC maturatio

50 lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at elevated levels in type 2 di

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

52 hat lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D2 (PGD2) metabolites produced

53 ns, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyz

54 evels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose

55 endogenous L-type prostaglandin D synthase (L-PGDS) in HeLa cells inhibited recycling of the prostag

56 role for lipocalin prostaglandin D synthase (L-PGDS) in the control of metabolic fuel utilization by

57 in lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, after E2 treatment, in the ve

58 ers lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycoprotein (AAG), transferrin

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

60 neuronal cells, lipocalin-type PGD synthase (L-PGDS) is detected in the macrophages infiltrated to at

61 calin-type prostaglandin D2 (PGD2) synthase (L-PGDS) interacts intracellularly with the GPCR DP1 in a

62 ter agonist-induced internalization and that L-PGDS overexpression had the opposite effect.

63 We conclude that L-PGDS plays an important role regulating insulin sensit

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

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

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

67 romatin immunoprecipitation assays show that L-PGDS induction was regulated positively by AP-1, but n

68 Our results show that L-PGDS KO mice become glucose-in-tolerant and insulin-re

69 Immunostaining showed that L-PGDS was expressed in the neurons of human myenteric a

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

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

72 In addition, only the L-PGDS KO mice developed nephropathy and an aortic thick

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

74 ieties (an improved technology), targeted to L-PGDS mRNA, (ii) scrambled sequence control oligos, or

75 Finally, whereas L-PGDS has been reported to be expressed primarily in ol

76 und that when WKY cells were pretreated with L-PGDS, insulin could actually induce apoptosis and fail