Relaxin is a peptide hormone whose A- and B-chains are derived by posttranslational cleavage from a single 185-amino acid preprorelaxin. Two genes in the human genome (H1 and H2) code for two polypeptides significantly different in amino acid sequence. The full spectrum of biological activities of these two polypeptides has not been examined, but transcription appears to be limited to the H2 relaxin gene in the human corpus luteum. Relaxin is also synthesized by the human decidua, placental trophoblast, and prostate gland; therefore, the expression of the human relaxin genes in these tissues has been examined using the reverse transcription polymerase chain reaction. The mRNA from decidua, placental trophoblast, and prostate was reverse transcribed and then amplified by polymerase chain reaction, using a series of oligonucleotide primers that were specific for but would not distinguish between human H1 and H2 relaxins. Using mRNA from these tissues, two amplified cDNA species were detected, whose identities were confirmed by Southern blots, HpaI and HpaII restriction enzyme analysis, and dideoxy sequencing. We have confirmed that the corpus luteum does not contain detectable H1 relaxin mRNA. However, we demonstrated for the first time relaxin H1 gene expression in the decidua, placental trophoblast, and prostate, and we have also shown that there are marked tissue differences in the relative amounts of expression of the H1 and H2 relaxin mRNA forms. The functional significance is unknown, but if both mRNAs are translated, differential expression of the two genes may result in tissue-specific differences in the production of these relaxins as well as in their binding and actions.

The production of prostaglandin E (PGE) and leukotriene B, (LTB,) by amnion was measured in v i m in 12 women delivered after spontaneous preterm labour and in 15 women delivered after spontaneous labour at term. T h e placenta and fetal membranes were examined histologically in all cases. PGE output (frnolirng dry weighti2 h) in the amnions from uncomplicated preterm deliveries was low (median 486, range 232-3203, n = 7) compared with the values obtained after spontaneous labour at term (5529, 1722-13 226, n = 15). In amnions from preterm deliveries complicated by acute chorioamnionitis or round ccll infiltration there was iiiassive release of PGE (15 242, 640, n = 5 ) which was accompanied by an increase in LTB, production. Inflammatory infiltration of the fetal membranes results in R hugc increaqe in PG production which could cause preterm labour.

Summary The production of prostaglandin E (PGE) by amnion, choriodecidua and placenta was measured in 45 women delivered after spontaneous preterm labour, in 10 women delivered electively preterm, in 30 women at elective caesarean section at term, and in 28 women after spontaneous labour at term. In the preterm labour group 24 women had normal placental histology, and gestational age was 34 (31–36) weeks (median and range); 18 women had evidence of chorioamnionitis and gestational age was significantly shorter, 30 (24–36) weeks; three other patients had placental abruption. In the absence of inflammatory infiltration of these tissues the highest PGE output (fmol/mg dry weight/2 h) was found after labour at term and the lowest after uncomplicated preterm labour: 2640 (360–15 580) (median and range) compared with 1414 (164–11 045) in amnion, 677 (100–3245) compared with 308 (39–1086) in choriodecidua, and 1200 (520–3022) compared with 578 (150–1859) in placenta, respectively. Tissues showing chorioamnionitis produced much higher outputs of PGE from amnion (12278, 1799–82 617) and from choriodecidua (1018, 216–11 768), but not from placenta (616, 89–4131). Chorioamnionitis seems to cause very early preterm labour by increasing PG production in the amnion and choriodecidua.

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