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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
8 mucosa showed significantly higher COX2 and L-PGDS mRNA expression, and significantly higher PGD2 le
15 nsating for a lack of PPARgamma2, we crossed L-PGDS KO mice to PPARgamma2 KO mice to generate Double
16 concentrations (20 mm) resulted in decreased L-PGDS expression in control cells but actually stimulat
17 R (DP1) promotes the activity of the enzyme (L-PGDS) that produces its agonist (PGD2) and in which th
18 this study, we report on the 50% increase in L-PGDS protein expression observed in vascular smooth mu
19 ridization revealed significant increases in L-PGDS expression in the arcuate and ventromedial nucleu
20 d focal adhesion kinase expression levels in L-PGDS KO vascular smooth muscle cells and controls.
22 der cold-acclimated conditions, mice lacking L-PGDS had elevated reliance on carbohydrate to provide
23 increases glucose utilization, mice lacking L-PGDS had improved glucose tolerance after high-fat fee
25 production, suggesting that H-PGDS, but not L-PGDS, mediates LPS-induced PGD(2) production in BMDM.
28 tion, we demonstrate differential effects of L-PGDS treatment on cell proliferation and apoptosis in
30 Together, our results identify induction of L-PGDS expression by inflammatory stimuli or bacterial i
32 Consistent with the concept that lack of L-PGDS increases glucose utilization, mice lacking L-PGD
33 erial infection, the regulatory mechanism of L-PGDS induction, and the protective role of L-PGDS expr
34 triguing possibility that E(2) modulation of L-PGDS plays a role in the regulation of sleep-wake stat
35 ng DKO mice we demonstrated a requirement of L-PGDS for maintenance of subcutaneous WAT (scWAT) funct
42 ts inhibitor HQL-79, but not lipocalin PGDS (L-PGDS) siRNA and its inhibitor AT-56, significantly att
47 lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at elevated levels in type 2 di
48 ng is lipocalin prostaglandin D(2) synthase (L-PGDS), which catalyzes the conversion of prostaglandin
49 hat lipocalin-type prostaglandin D synthase (L-PGDS) and prostaglandin D2 (PGD2) metabolites produced
50 ns, Lipocalin-type prostaglandin D synthase (L-PGDS) expression by neurons and glial cells was analyz
51 evels of Lipocalin prostaglandin D synthase (L-PGDS) expression in BAT and subcutaneous white adipose
52 role for lipocalin prostaglandin D synthase (L-PGDS) in the control of metabolic fuel utilization by
53 in lipocalin-type prostaglandin D synthase (L-PGDS) transcript levels, after E2 treatment, in the ve
54 ers lipocalin-like prostaglandin D synthase (L-PGDS), alpha(1) -acid glycoprotein (AAG), transferrin
55 Lipocalin-type prostaglandin D2 synthase (L-PGDS) has recently been linked to a variety of pathoph
56 neuronal cells, lipocalin-type PGD synthase (L-PGDS) is detected in the macrophages infiltrated to at
57 calin-type prostaglandin D2 (PGD2) synthase (L-PGDS) interacts intracellularly with the GPCR DP1 in a
60 , we demonstrate, immunocytochemically, that L-PGDS is also expressed in a population of VLPO neurons
62 romatin immunoprecipitation assays show that L-PGDS induction was regulated positively by AP-1, but n
65 Taken together, these results suggest that L-PGDS plays an important role in the regulation of gluc
66 Adipocytes were significantly larger in the L-PGDS KO mice compared with controls on the same diets.
69 ieties (an improved technology), targeted to L-PGDS mRNA, (ii) scrambled sequence control oligos, or
71 und that when WKY cells were pretreated with L-PGDS, insulin could actually induce apoptosis and fail
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