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Prostaglandin E (prostaglandin + e)
Kinds of Prostaglandin E Terms modified by Prostaglandin E Selected AbstractsPrecise mapping of breakpoints in conserved synteny between human chromosome 1 and pig chromosomes 4, 6 and 9ANIMAL GENETICS, Issue 2 2002H. S. Sun Previous comparative mapping suggested that at least five pig chromosomes (Sscr4, 6, 9, 10 and 14) share homology with human chromosome 1 (Hsap1). A significant quantitative trait loci (QTL) for fat deposition has been identified on Sscr4 that appears to be near the junction region between Sscr4 and Sscr9 relative to Hsap1. It is of interest to define the boundaries of conserved synteny between pig chromosomes and Hsap1 to use human map information to identify putative comparative positional candidates for this QTL. Eleven genes, including Janus kinase 1 (JAK1), Prostaglandin E receptor3 (PTGER3), urate oxidase (UOX), coagulation factor 3 (F3), vascular cell adhesion molecule 1 (VCAM1), ribosomal protein L5 (RPL5), POU domain, class 2, transcription factor 1 (POU2F1), coagulation factor 5 (F5), Prostaglandin endoperoxide synthase-2 (PTGS2), myosin binding protein H (MYBPH) and Antithrombin III (SERPINC1), were selected to refine the boundaries of the blocks of conserved synteny between Hsap1 and pig chromosomes. Pig sequence tagged sites (STSs) were developed and used to physically map these 11 genes using a somatic cell hybrid panel. Eight loci have been mapped by using fluorescent in situ hybridization (FISH) to improve map resolution. Heterologous FISH was used to refine the location of VCAM1 on human chromosomes. In addition, human yeast artificial chromosomes (YACs) were mapped by heterologous FISH on pig metaphases to refine the boundaries of the regions of homology between Sscr4 and Sscr9 on Hsap1. Results from this study suggest the precise break in conserved synteny on Hsap1 corresponding to the Sscr4/6 and Sscr4/9 transitions are most likely on the Hsap1p22 and Hsap1q24,25 regions, respectively. Further, our data predict that Hsap1q21,24 is a candidate region for the backfat QTL localized to Sscr4. [source] NKT cells are dispensable in the induction of oral tolerance but are indispensable in the abrogation of oral tolerance by prostaglandin EEUROPEAN JOURNAL OF IMMUNOLOGY, Issue 1 2003Ryotaro Ishimitsu Abstract NK1.1+ ,,, T cells (NKT cells) regulate the Th1/Th2 balance in response to dietary Ag, which may be involved in regulation of oral tolerance. OVA-specific IgE and IgG1 Ab levels were significantly lower following an i.p. injection of OVA (in CFA) in C57BL/6 mice orally given a single, high dose (25,mg) of OVA than in those orally given PBS. The oral tolerance was normally induced in J,281,/, mice which lack V,14+ NKT cells, suggesting that NKT cells are dispensable for induction of oral tolerance. Treatment with PGE1 or PGE2 abrogated the oral tolerance in J,281+/+ mice; this abrogation was accompanied by an OVA-specific Th2-dominant response. The abrogation of oral tolerance by PGE1 was not evident in J,281,/, mice. Treatment with PGE1 induced an early increase in IL-4 production by liver NKT cells in normal mice and neutralization of the early IL-4 by administration of anti-IL-4 mAb abolished PGE1 -induced abrogation of oral tolerance. These results suggest that liver NKT cells producing IL-4 are responsible for the down-regulation of oral tolerance that is caused by the PGE molecules. [source] CREB-dependent cyclooxygenase-2 and microsomal prostaglandin E synthase-1 expression is mediated by protein kinase C and calciumJOURNAL OF CELLULAR BIOCHEMISTRY, Issue 6 2006Hung Pham Abstract Cellular production of prostaglandins (PGs) is controlled by the concerted actions of cyclooxygenases (COX) and terminal PG synthases on arachidonic acid in response to agonist stimulation. Recently, we showed in an ileal epithelial cell line (IEC-18), angiotensin II-induced COX-2-dependent PGI2 production through p38MAPK, and calcium mobilization (J. Biol. Chem. 280: 1582,1593, 2005). Agonist binding to the AT1 receptor results in activation of PKC activity and Ca2+ signaling but it is unclear how each pathway contributes to PG production. IEC-18 cells were stimulated with either phorbol-12,13-dibutyrate (PDB), thapsigargin (TG), or in combination. The PG production and COX-2 and PG synthase expression were measured. Surprisingly, PDB and TG produced PGE2 but not PGI2. This corresponded to induction of COX-2 and mPGES-1 mRNA and protein. PGIS mRNA and protein levels did not change. Activation of PKC by PDB resulted in the activation of ERK1/2, JNK, and CREB whereas activation of Ca2+ signaling by TG resulted in the delayed activation of ERK1/2. The combined effect of PKC and Ca2+ signaling were prolonged COX-2 and mPGES-1 mRNA and protein expression. Inhibition of PKC activity, MEK activity, or Ca2+ signaling blocked agonist induction of COX-2 and mPGES-1. Expression of a dominant negative CREB (S133A) blocked PDB/TG-dependent induction of both COX-2 and mPGES-1 promoters. Decreased CREB expression by siRNA blocked PDB/TG-dependent expression of COX-2 and mPGES-1 mRNA. These findings demonstrate a coordinated induction of COX-2 and mPGES-1 by PDB/TG that proceeds through PKC/ERK and Ca2+ signaling cascades, resulting in increased PGE2 production. J. Cell. Biochem. © 2006 Wiley-Liss, Inc. [source] Triclosan reduces microsomal prostaglandin E synthase-1 expression in human gingival fibroblastsJOURNAL OF CLINICAL PERIODONTOLOGY, Issue 1 2005M. Mustafa Abstract Objective: The effect of triclosan (2,4,4,-trichloro-2,-hydroxydiphenyl ether) on the expression of cyclooxygenase-2 (COX-2) and microsomal prostaglandin E synthase-1 (mPGES-1) and on the translocation of the nuclear factor- ,B (NF- ,B) in relation to prostaglandin E2 (PGE2) production was investigated in human gingival fibroblasts challenged with tumor necrosis factor , (TNF,). Methods: Fibroblasts were established from gingival biopsies obtained from six children. COX-2 mRNA and protein expression was quantified using mRNA quantitation and enzyme immunometric assay kits. mPGES-1 mRNA was analysed by RT-PCR, mPGES-1 protein and NF-,B translocation by immunoblotting. PGE2 was determined by radioimmunoassay. Results: The cytokine TNF, enhanced the expression of mRNA as well as the protein levels of both COX-2 and mPGES-1 and subsequently the production of PGE2 in gingival fibroblasts. Treatment of gingival fibroblasts with triclosan (1 ,g/ml) significantly reduced the stimulatory effect of TNF, (10 ng/ml) on the expression of mPGES-1 at both the mRNA and the protein level by an average of 21% and 43%, respectively, and subsequently the production of PGE2 (p<0.01). Triclosan did not, however, affect the translocation of NF- ,B or the expression of COX-2 in TNF,- stimulated cells. Conclusion: The results show that triclosan reduces the augmented biosynthesis of PGE2 by inhibiting the mRNA and the protein expression of mPGES-1 in gingival fibroblasts. This finding may partly explain the anti-inflammatory effect of the agent previously reported in clinical studies. [source] Microsomal prostaglandin E synthase-1 and 5-lipoxygenase: potential drug targets in cancerJOURNAL OF INTERNAL MEDICINE, Issue 1 2010O. Rådmark Abstract., Rådmark O, Samuelsson B (Karolinska Institutet, Stockholm, Sweden). Microsomal prostaglandin Esynthase-1 and 5-lipoxygenase: potential drug targets in cancer (Review). J Intern Med 2010; 268:5,14. There is strong evidence for a role of prostaglandin (PG)E2 in cancer cell proliferation and tumour development. In PGE2 biosynthesis, cyclooxygenases (COX-1/2) convert arachidonic acid to PGH2, which can be isomerized to PGE2 by PGE synthases, including microsomal PGE synthase-1 (MPGES-1). Data describing genetic deletions of MPGES-1 are reviewed. The results suggest that MPGES-1 is an alternative therapeutic target for cancer cells and tumours that express this enzyme. Several compounds that target COX-2 or MPGES-1 also inhibit 5-lipoxygenase. This may be advantageous for treatment of some forms of cancer. [source] Detection of fascin and CCR-7 positive mature dendritic cells in oral lichen planusJOURNAL OF ORAL PATHOLOGY & MEDICINE, Issue 4 2009Shotaro Mukae Background:, Dendritic cells (DC) play a crucial role in the pathogenesis of oral lichen planus (OLP) with respect to antigens presented to T cells. We performed immunohistochemical analysis to elucidate the process of activation of DC in OLP. Methods:, Thirty biopsy specimens were obtained from the patients with OLP. The expressions of CD1a, Langerin, S-100, fascin, chemokine receptor-7 (CCR-7), D2-40, cyclooxygenase-2 (COX-2), and microsomal prostaglandin E synthase-1 (mPGES-1) in DC from OLP and disease free control were investigated using specific antibodies. The distribution and number (1 mm2) of DC were assessed in the intra-epithelium and the submucosa specimens. Correlation between the number of DC and epithelium thickness was also determined. Result:, Immature DC (Langerin+, CD1a+, and S-100+) were identified in the epithelia from OLP patients and control, though the numbers of Langerin+ and CD1a+ positive cells were decreased in the OLP samples as compared to the control. Mature DC (fascin+) were identified in the submucosa specimens, not found in the epithelium from OLP or control. Double immunostaining revealed DC positive for fascin and CCR-7 in the submucosa, which had migrated into D2-40+ lymph vessels. Furthermore, keratinocytes expressed both Prostaglandin E2 (PGE2) converting enzymes, COX-2, and mPGES-1, indicating PGE2 synthesis in the epithelial layer of the OLP specimens. Conclusion:, Our results indicate that DC change from immature to mature in the epithelium and are then drawn out to the submucosa. We demonstrate that mature DC localized in the submucosa, it consequently migrates into lymph vessels. This maturation process of DC is an important immunopathological feature of OLP. [source] Outcomes for subsequent pregnancy in women who have undergone misoprostol mid-trimester termination of pregnancyAUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 2 2009Vadim MIRMILSTEIN In Australia, the most common method of mid-trimester termination of pregnancy (TOP) is by medical induction with the prostaglandin E 1 analog misoprostol. This study was undertaken to compare the pregnancy outcomes of women who had undergone a misoprostol mid-trimester TOP in their last pregnancy with those of a similar cohort of women without a history of misoprostol TOP. This study suggests a possibility that medical mid-trimester TOP with misoprostol increases the risk of preterm or very preterm delivery in a subsequent pregnancy but larger studies are needed to confirm or dismiss this. [source] | |||||||||||||