OBJECTIVES: The purpose of this paper is to elucidate the roles of phospholipase A(2) (PLA(2)), cyclooxygenase-2 (COX-2), and prostaglandin I(2) (PGI(2)) synthase in pregnancy induced hypertension (PIH). METHODS: In placentas from normal pregnant women and pregnant women with severe PIH, the enzyme expression of PLA(2), COX-2, and PGI(2) synthase was measured using real time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The expression of each enzyme was compared between normal (n=12) and PIH (n=12) groups. The expression levels of COX-2 and PGI(2) synthase during PIH pregnancy were significantly decreased to about 51% and 68%, respectively, of their values in normal pregnancy. However, the expression of PLA(2) was hardly changed by PIH. CONCLUSIONS: The decreases in COX-2 and PGI(2) synthase expression in severe PIH placentas may be causal factors in the disruption of the PGI(2)-thromboxane A(2) (TXA(2)) balance in favor of TXA(2). The decrease in COX-2 was more marked than that of PGI(2) synthase.
OBJECTIVES: The purpose of this paper is to elucidate the roles of phospholipase A(2) (PLA(2)), cyclooxygenase-2 (COX-2), and prostaglandin I(2) (PGI(2)) synthase in pregnancy induced hypertension (PIH). METHODS: In placentas from normal pregnant women and pregnant women with severe PIH, the enzyme expression of PLA(2), COX-2, and PGI(2) synthase was measured using real time reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: The expression of each enzyme was compared between normal (n=12) and PIH (n=12) groups. The expression levels of COX-2 and PGI(2) synthase during PIH pregnancy were significantly decreased to about 51% and 68%, respectively, of their values in normal pregnancy. However, the expression of PLA(2) was hardly changed by PIH. CONCLUSIONS: The decreases in COX-2 and PGI(2) synthase expression in severe PIH placentas may be causal factors in the disruption of the PGI(2)-thromboxane A(2) (TXA(2)) balance in favor of TXA(2). The decrease in COX-2 was more marked than that of PGI(2) synthase.