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

Abstract

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 ...

Source of angiopoietin-2 in the sera of women during pregnancy

“…Furthermore, a reduction of COX-2 expression was observed in pregnancy induced hypertension (Okawara et al, 2009). It would therefore, be of interest to investigate the correlation of Ang-2 secretion and COX-2 (and its downstream elements) expression during normal pregnancy.…”

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

“…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.…”

An imbalance of COX level is not related to placental abruption

“…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.…”