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15-epi-lipoxin A4 reduces the mortality of prematurely born pups in a mouse model of infection-induced preterm birth.

Rinaldi SF, Catalano RD, Wade J, Rossi AG, Norman JE - Mol. Hum. Reprod. (2015)

Bottom Line: There are currently few effective therapies and therefore an urgent need for novel treatments.Although there is much focus on trying to alter gestation of delivery, the primary aim of preterm birth prevention therapies should be to reduce prematurity related mortality and morbidity.Quantitative real-time (QRT)-PCR analysis of utero-placental tissues harvested 6 h post-treatment demonstrated that 15-epi-lipoxin A4 treatment increased Ptgs2 expression in the uterus, placenta and fetal membranes (P < 0.05) and decreased 15-Hpgd expression (P < 0.05) in the placenta and uterus, suggesting that 15-epi-lipoxin A4 may regulate the local production and activity of prostaglandins.

View Article: PubMed Central - PubMed

Affiliation: MRC Centre for Reproductive Health and Tommy's Centre for Maternal and Fetal Health, University of Edinburgh, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK s.rinaldi@ed.ac.uk.

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Effect of pretreatment with 15-epi-lipoxin A4 on mRNA expression of Ptgs2 and 15-Hpgd in the utero-placental tissues. Uterus, placenta and fetal membranes were collected 6 h post-surgery from mice pretreated with vehicle (n = 3) or 2.5 μg 15-epi-lipoxin A4 (n = 4), prior to intrauterine PBS; and in mice pretreated with vehicle (n = 5), 0.25 μg 15-epi-lipoxin A4 (n = 5) or 2.5 μg 15-epi-lipoxin A4 (n = 5), prior to intrauterine LPS administration. The mRNA expression of Ptgs2 and 15-Hpgd was quantified by quantitative real-time PCR. (A) Uterine expression. (B) Placental expression. (C) Expression in the fetal membranes. Data presented as mean fold change ± SEM (error bars); *P < 0.05, **P < 0.01, ***P < 0.001, compared with vehicle; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with LPS.
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GAU117F3: Effect of pretreatment with 15-epi-lipoxin A4 on mRNA expression of Ptgs2 and 15-Hpgd in the utero-placental tissues. Uterus, placenta and fetal membranes were collected 6 h post-surgery from mice pretreated with vehicle (n = 3) or 2.5 μg 15-epi-lipoxin A4 (n = 4), prior to intrauterine PBS; and in mice pretreated with vehicle (n = 5), 0.25 μg 15-epi-lipoxin A4 (n = 5) or 2.5 μg 15-epi-lipoxin A4 (n = 5), prior to intrauterine LPS administration. The mRNA expression of Ptgs2 and 15-Hpgd was quantified by quantitative real-time PCR. (A) Uterine expression. (B) Placental expression. (C) Expression in the fetal membranes. Data presented as mean fold change ± SEM (error bars); *P < 0.05, **P < 0.01, ***P < 0.001, compared with vehicle; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with LPS.

Mentions: In the uterus, Ptgs2 expression was significantly elevated in response to 2.5 µg 15-epi-lipoxin A4 alone (P < 0.01), LPS alone (P < 0.01), and 0.25 µg and 2.5 µg 15-epi-lipoxin A4 + LPS (P < 0.001; Fig. 3A), compared with the vehicle control group. Co-treatment with 2.5 µg 15-epi-lipoxin A4 and LPS also significantly increased uterine Ptgs2 expression compared with treatment with LPS alone (P < 0.05; Fig. 3A). Conversely, uterine 15-Hpgd expression was significantly reduced in mice treated with 2.5 µg 15-epi-lipoxin A4 prior to intrauterine PBS, compared with vehicle (P < 0.01) and LPS alone (P < 0.05). LPS alone did not significantly alter 15-Hpgd expression; however, mice treated with 0.25 µg 15-epi-lipoxin A4 + LPS and 2.5 µg 15-epi-lipoxin A4 + LPS had significantly reduced uterine 15-Hpgd expression, compared with the vehicle group (P < 0.001). Additionally pretreatment with 0.25 µg 15-epi-lipoxin A4 and 2.5 µg 15-epi-lipoxin A4 prior to intrauterine LPS, significantly reduced uterine expression of 15-Hpgd, compared with LPS alone (P < 0.001; Fig. 3A).Figure 3


15-epi-lipoxin A4 reduces the mortality of prematurely born pups in a mouse model of infection-induced preterm birth.

Rinaldi SF, Catalano RD, Wade J, Rossi AG, Norman JE - Mol. Hum. Reprod. (2015)

Effect of pretreatment with 15-epi-lipoxin A4 on mRNA expression of Ptgs2 and 15-Hpgd in the utero-placental tissues. Uterus, placenta and fetal membranes were collected 6 h post-surgery from mice pretreated with vehicle (n = 3) or 2.5 μg 15-epi-lipoxin A4 (n = 4), prior to intrauterine PBS; and in mice pretreated with vehicle (n = 5), 0.25 μg 15-epi-lipoxin A4 (n = 5) or 2.5 μg 15-epi-lipoxin A4 (n = 5), prior to intrauterine LPS administration. The mRNA expression of Ptgs2 and 15-Hpgd was quantified by quantitative real-time PCR. (A) Uterine expression. (B) Placental expression. (C) Expression in the fetal membranes. Data presented as mean fold change ± SEM (error bars); *P < 0.05, **P < 0.01, ***P < 0.001, compared with vehicle; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with LPS.
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GAU117F3: Effect of pretreatment with 15-epi-lipoxin A4 on mRNA expression of Ptgs2 and 15-Hpgd in the utero-placental tissues. Uterus, placenta and fetal membranes were collected 6 h post-surgery from mice pretreated with vehicle (n = 3) or 2.5 μg 15-epi-lipoxin A4 (n = 4), prior to intrauterine PBS; and in mice pretreated with vehicle (n = 5), 0.25 μg 15-epi-lipoxin A4 (n = 5) or 2.5 μg 15-epi-lipoxin A4 (n = 5), prior to intrauterine LPS administration. The mRNA expression of Ptgs2 and 15-Hpgd was quantified by quantitative real-time PCR. (A) Uterine expression. (B) Placental expression. (C) Expression in the fetal membranes. Data presented as mean fold change ± SEM (error bars); *P < 0.05, **P < 0.01, ***P < 0.001, compared with vehicle; #P < 0.05, ##P < 0.01, ###P < 0.001, compared with LPS.
Mentions: In the uterus, Ptgs2 expression was significantly elevated in response to 2.5 µg 15-epi-lipoxin A4 alone (P < 0.01), LPS alone (P < 0.01), and 0.25 µg and 2.5 µg 15-epi-lipoxin A4 + LPS (P < 0.001; Fig. 3A), compared with the vehicle control group. Co-treatment with 2.5 µg 15-epi-lipoxin A4 and LPS also significantly increased uterine Ptgs2 expression compared with treatment with LPS alone (P < 0.05; Fig. 3A). Conversely, uterine 15-Hpgd expression was significantly reduced in mice treated with 2.5 µg 15-epi-lipoxin A4 prior to intrauterine PBS, compared with vehicle (P < 0.01) and LPS alone (P < 0.05). LPS alone did not significantly alter 15-Hpgd expression; however, mice treated with 0.25 µg 15-epi-lipoxin A4 + LPS and 2.5 µg 15-epi-lipoxin A4 + LPS had significantly reduced uterine 15-Hpgd expression, compared with the vehicle group (P < 0.001). Additionally pretreatment with 0.25 µg 15-epi-lipoxin A4 and 2.5 µg 15-epi-lipoxin A4 prior to intrauterine LPS, significantly reduced uterine expression of 15-Hpgd, compared with LPS alone (P < 0.001; Fig. 3A).Figure 3

Bottom Line: There are currently few effective therapies and therefore an urgent need for novel treatments.Although there is much focus on trying to alter gestation of delivery, the primary aim of preterm birth prevention therapies should be to reduce prematurity related mortality and morbidity.Quantitative real-time (QRT)-PCR analysis of utero-placental tissues harvested 6 h post-treatment demonstrated that 15-epi-lipoxin A4 treatment increased Ptgs2 expression in the uterus, placenta and fetal membranes (P < 0.05) and decreased 15-Hpgd expression (P < 0.05) in the placenta and uterus, suggesting that 15-epi-lipoxin A4 may regulate the local production and activity of prostaglandins.

View Article: PubMed Central - PubMed

Affiliation: MRC Centre for Reproductive Health and Tommy's Centre for Maternal and Fetal Health, University of Edinburgh, Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh EH16 4TJ, UK s.rinaldi@ed.ac.uk.

Show MeSH
Related in: MedlinePlus