Cyclooxygenase-1 and -2 in human placenta and placental bed after normal and pre-eclamptic pregnancies

Wetzka, B.; Nüsing, Rolf M.; Charnock-Jones, D. Stephen; Schäfer, Wolfgang; Zahradnik, H. P.; Smith, Stephen K.

doi:10.1093/humrep/12.10.2313

Cited by 43 publications

(33 citation statements)

References 24 publications

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“…In pregnancies complicated by both IUGR and PE (IUGR-PE), AA was not significantly higher than in controls despite significantly lower percentage LA. Although this might be simply related to the failure to reach statistical power, another possible speculation is related to the increased arachidonic employment in the synthesis of molecules liable to the pathogenesis of PE, such as thromboxane (32). PE and IUGR are two pathological conditions involving an inflammatory process probably beginning in the placenta during the first stages of pregnancy (16).…”

Section: Discussionmentioning

confidence: 99%

“…Increases of NEFA and triglycerides in the fetal circulation of only IUGR-PE could be the reflection of changes in placental lipase activities (31)(32)(33)(34)(35)(36)(37)(38)(39)(40)(41)(42)(43) in this pathological condition characterized by placental insufficiency but also by a vascular damage in which the atherogenic role of lipids and lipoperoxidation have been well established (18).…”

Section: Discussionmentioning

confidence: 99%

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Maternal and Fetal Fatty Acid Profile in Normal and Intrauterine Growth Restriction Pregnancies With and Without Preeclampsia

et al. 2008

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ABSTRACT:The aim of this study was to evaluate maternal and fetal lipid profile in intrauterine growth restriction (IUGR) pregnancies with and without preeclampsia (PE). Thirteen normal pregnancies studied during the third trimester (control M) and 29 at elective cesarean section (control CS) were compared with 18 pregnancies complicated by IUGR (IUGR only) and with seven pregnancies complicated by both IUGR and PE (IUGR-PE). Total plasma fatty acids, triglycerides, cholesterol, and nonesterified fatty acids (NEFA) were determined in maternal and fetal plasma. Nutritional intake was analyzed. IUGR only mothers had lower percentage of linoleic acid (LA) and higher arachidonic acid (AA) than controls, partly explained by higher AA dietary intake. Higher levels of NEFA were observed both in IUGR only and in IUGR-PE mothers whereas triglyceride levels were increased in IUGR-PE mothers only. In IUGR-PE fetuses, LA and AA were significantly decreased, whereas triglyceride and NEFA concentrations were significantly increased compared with normal fetuses. In conclusion, IUGR only is associated with altered fatty acids profile not completely accounted by dietary changes. We hypothesize that the differences observed in IUGR with PE for triglycerides and other lipids could be related to a difference in maternal phenotype. (Pediatr Res 64: 615-620, 2008)

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Maternal and Fetal Fatty Acid Profile in Normal and Intrauterine Growth Restriction Pregnancies With and Without Preeclampsia

et al. 2008

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“…Numerous studies have shown that Cox-2 is highly expressed in endometriosis (Ota et al 2001, Chishima et al 2002. Other studies show that Cox-2 is strongly expressed in endometrial adenocarcinomas (Uotila et al 2002), but not in preeclampsia (Wetzka et al 1997). …”

Section: Cyclooxygenase-2 (Cox-2)mentioning

confidence: 91%

Animal models of implantation

Lee

DeMayo²

2004

Reproduction

240

155

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Implantation is an intricately timed event necessary in the process of viviparous birth that allows mammals to nourish and protect their young during early development. Human implantation begins when the blastocyst both assumes a fixed position in the uterus and establishes a more intimate relationship with the endometrium. Due to the impracticalities of studying implantation in humans, animal models are necessary to decipher the molecular and mechanical events of this process. This review will discuss the differences in implantation between different animal models and describe how these differences can be utilized to investigate discrete implantation stages. In addition, factors that have been shown to be involved in implantation in the human and other various animal models including growth factors, cytokines, modulators of cell adhesion, and developmental factors will be discussed, and examples from each will be given.

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“…Wetzka et al reported that there were no significant differences in COX-1 and COX-2 expression between precritical and postcritical PIH sufferers. 8) On the other hand, Borekci et al reported that the COX-1 and COX-2 activity in severe and mild PIH patients was significantly lower than that in a normal pregnant group. 9) No differences in PGI 2 synthase or TXA 2 synthase were reported between normal and PIH pregnant groups.…”

Section: Discussionmentioning

confidence: 97%

Examination of the Expression of Cyclooxygenase-2 in Placenta Villi from Sufferers of Pregnancy Induced Hypertension

Okawara

Matsuoka

Hashimoto

et al. 2009

Biological & Pharmaceutical Bulletin

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Pregnancy induced hypertension (PIH) causes hypertensive cerebropathy, deep vein thrombosis, pulmonary embolismlung edema, intrauterine growth retardation, and premature delivery. It is therefore considered to be a serious disease that affects both mother and fetus. However, the mechanism through which PIH induces its clinical symptoms is unknown. At first, damage to vascular endothelial cells induces vasoconstriction and hemoconcentration, resulting in fetoplacental circulation dysfunction. Then, clinical symptoms such as hypertension and protein urea are induced.As described above, the damage caused to vascular endothelial cells is the main pathogenic factor in PIH and results in decreased concentrations of vasodilatatory factors. Therefore, it is assumed that circulation homeostasis is disrupted. The prostaglandin I 2 (PGI 2 )-thromboxane A 2 (TXA 2 ) adjustment system is present in many circulation control systems. Prostaglandin I 2 is synthesized in the endovascular system and acts as a vasodilator in addition to its inhibitory effect on platelet aggregation. In contrast, TXA 2 is synthesized by platelets, acts as a vasoconstrictor, and induces platelet aggregation. Furthermore, PGI 2 and TXA 2 are synthesized from the same precursor, arachidonic acid. These prostaglandins, which have opposite effects, are synthesized in close proximity to each other, such as in blood vessels and platelets, and maintain circulation homeostasis. Therefore, the PGI 2 -TXA 2 balance is considered to be a complex mechanism for circulation control. Additionally, PGI 2 and TXA 2 are synthesized in the placenta, umbilical vein, uterine blood vessel, amnion, chorionic villi, and decidua. The PGI 2 -TXA 2 balance is considered to be very important in the fetoplacental circulating system; therefore, an imbalance in this system may play an important part in PIH pathogenesis.1) In another report, production of PGI 2 was decreased and TXA 2 was increased in the blood, urine, and tissues of PIH maternal and fetal tissues, indicating that the PGI 2 -TXA 2 equilibrium in these tissues is pushed towards TXA 2 . Similar results have also been reported in umbilical and placental tissue.2) These differences may depend on (1) the activity of prostaglandin production enzymes, (2) the content of these enzymes, and (3) the activity of inhibitors for these enzymes.Satoh et al. reported that the activity of enzymes such as cyclooxygenase-2 (COX-2), which takes part in the synthesis of PGI 2 , is decreased in the endothelium of the umbilical vein in patients with severe PIH, resulting in an imbalance in the PGI 2 -TXA 2 system that leads to TXA 2 predominance. 3)However, in their report, no distinction between COX-1 and COX-2 was made because the isozymes of COX had not yet been discovered. In addition, Keirse et al. determined the contents of COX and PGI 2 synthetase using an immunoradiometric assay with monoclonal antibody. 4,5) In their report, COX was induced and increased with increasing gestational age, but there was no difference in the level ...

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Cyclooxygenase-1 and -2 in human placenta and placental bed after normal and pre-eclamptic pregnancies

Cited by 43 publications

References 24 publications

Maternal and Fetal Fatty Acid Profile in Normal and Intrauterine Growth Restriction Pregnancies With and Without Preeclampsia

Maternal and Fetal Fatty Acid Profile in Normal and Intrauterine Growth Restriction Pregnancies With and Without Preeclampsia

Animal models of implantation

Examination of the Expression of Cyclooxygenase-2 in Placenta Villi from Sufferers of Pregnancy Induced Hypertension

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