Placental tissue cyclo-oxygenase 1 and 2 in pre-eclamptic and normal pregnancy

Borekci, Bunyamin; Aksoy, Hülya; Toker, Aysun; Özkan, Asuman Deveci

doi:10.1016/j.ijgo.2006.06.016

Cited by 15 publications

(9 citation statements)

References 19 publications

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“…A precise balance between COX-negative and COX-positive cells is necessary to ensure the adequate production of PGs and to allow a physiological evolution of pregnancy [ 48 ]. Placental COX1 and COX2 activities were reported to be decreased in case of PE [ 90 , 91 ], while fetal COX2 polymorphism was suspected to contribute to the development of FGR [ 92 ]. The role of COXs in placental abruption remains unclear and the research is still ongoing.…”

Section: Resultsmentioning

confidence: 99%

Molecular Changes on Maternal–Fetal Interface in Placental Abruption—A Systematic Review

Bączkowska

Zgliczyńska

Faryna³

et al. 2021

IJMS

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Placental abruption is the separation of the placenta from the lining of the uterus before childbirth. It is an infrequent perinatal complication with serious after-effects and a marked risk of maternal and fetal mortality. Despite the fact that numerous placental abruption risk factors are known, the pathophysiology of this issue is multifactorial and not entirely clear. The aim of this review was to examine the current state of knowledge concerning the molecular changes on the maternal–fetal interface occurring in placental abruption. Only original research articles describing studies published in English until the 15 March 2021 were considered eligible. Reviews, book chapters, case studies, conference papers and opinions were excluded. The systematic literature search of PubMed/MEDLINE and Scopus databases identified 708 articles, 22 of which were analyzed. The available evidence indicates that the disruption of the immunological processes on the maternal–fetal interface plays a crucial role in the pathophysiology of placental abruption. The features of chronic non-infectious inflammation and augmented immunological cytotoxic response were found to be present in placental abruption samples in the reviewed studies. Various molecules participate in this process, with only a few being examined. More advanced research is needed to fully explain this complicated process.

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Section: Resultsmentioning

confidence: 99%

Molecular Changes on Maternal–Fetal Interface in Placental Abruption—A Systematic Review

Bączkowska

Zgliczyńska

Faryna³

et al. 2021

IJMS

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“…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. 10) In villi and deciduas, no Gene PLA 2 Forward 5Ј-GAC TGG AGA GCC ACC CTG AAG Reverse 5Ј-CGG CGT TCA GGT ACG TGT C COX-2 Forward 5Ј-GCG AGG GCC AGC TTT CA Reverse 5Ј-CAG AGT TTC ACC GTA AAT ATG ATT TAA PGI 2 Forward 5Ј-CCA CGC ACC CAT GAA AGC synthase Reverse 5Ј-TGG CGA AAG GTG TGG AAG A differences in COX-1 and COX-2 expression were found between normal and PIH pregnant groups, but the TXA 2 synthase content was increased in the PIH pregnant group.…”

Section: Discussionmentioning

confidence: 94%

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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“…COX 1 and COX 2 activities have been reported to be decreased in placental homogenates of preeclamptic pregnancies,28 29 and fetal COX 2 polymorphism has been found to influence the rate of malperfusion, ischaemia and possibly the development of IUGR 30. Both preeclampsia and IUGR have been shown to be related to inadequate trophoblast invasion and to failure of physiological spiral artery changes 31.…”

Section: Discussionmentioning

confidence: 99%

An imbalance of COX level is not related to placental abruption

et al. 2011

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Placental tissue cyclo-oxygenase 1 and 2 in pre-eclamptic and normal pregnancy

Abstract: These results suggest that COX-1 and COX-2 activities are decreased in the placental tissue of women with pre-eclampsia, probably by oxidative stress.

Cited by 15 publications

References 19 publications

Molecular Changes on Maternal–Fetal Interface in Placental Abruption—A Systematic Review

Molecular Changes on Maternal–Fetal Interface in Placental Abruption—A Systematic Review

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

An imbalance of COX level is not related to placental abruption

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