Prostaglandins play a central role in the stimulation and maintenance of both term and
preterm labor.
15-Hydroxyprostaglandin dehydrogenase (PGDH), localized primarily to chorion trophoblasts, is the key
enzyme responsible for the metabolism of
prostaglandins. In preterm chorion, levels of PGDH
protein and activity were lower when compared to term and were further reduced with the presence of
infection, but effects of subclinical
inflammation and membrane
rupture on PGDH expression are not known. Our objectives were (1) to determine the relative expression of PGDH in amnion and chorion and (2) to determine the effect of preterm premature
rupture of membranes (
PPROM) and (3) subclinical
inflammation on PGDH
protein expression in preterm fetal membranes. Fetal membranes were collected from women with idiopathic
preterm labor. Patients were divided into
preterm birth (1) <32 weeks with
PPROM (n = 6), (2) <32 weeks with intact membranes (n = 11), (3) >or=32 and <37 weeks with
PPROM (n = 10), and (4) >or=32 and <37 weeks with intact membranes (n = 10). Different
antibodies were used to detect
protein expression and localization of PGDH in amnion and chorion from these patients using both Western blotting and immunohistochemistry. Antibody T (AbT) localized PGDH to chorion trophoblasts, whereas antibody C (AbC) detected immunoreactive (ir) PGDH predominantly in the amnion mesenchyme. By Western blot, AbT showed a stronger 29-kDa ir-PGDH band whereas with AbC, a stronger 55-kDa ir-PGDH signal was detected. 55-kDa ir-PGDH was significantly higher in
PPROM amnion, specifically in the <32 weeks group (P < .05) and with
PPROM >24 hours (P < .05). No change was detected in the 29-kDa ir-PGDH in either amnion or chorion with gestational age or the presence and absence of
PPROM. In addition, neither form of ir-PGDH was altered significantly with or without subclinical
inflammation. ir-PGDH is detectable in both chorion trophoblasts and amnion, especially in the mesenchyme; however, the predominant form of the
enzyme differs in the 2 tissues.
PPROM and subclinical
inflammation do not appear to affect the levels of 29-kDa ir-PGDH
protein in the fetal membranes. The differential expression of 55-kDa ir-PGDH in preterm amnion with and without
PPROM supports the need for a better understanding of the different forms of PGDH.