Preterm birth comprises of several distinct clinical phenotypes. The commonalities and differences of the genes altered in the different phenotypes of preterm labour (PTL) have yet to be elucidated.
Myometrial biopsies were collected during caesarean section from women in preterm no labour (PNL; n = 26), preterm labour (chorioamnionitis, placental abruption, polyhydramnios and idiopathic; n = 11, 6, 16 and 4 respectively), preterm twins (NL and L; n = 12), term no labour (n = 18), term early labour (EAL, <3 cm dilatation; n = 10) and established labour (ESL, ≥3 cm dilatation; n = 12). Samples were rapidly frozen at -800C. Total RNA was extracted using RNeasy kit from Qiagen and converted to cDNA. Copy numbers of PGHS-2, CXCL-8, oxytocin receptor, IL-6, connexin 43 and GAPDH were measured by qPCR using Rotor-GeneTM (Corbett Research, Australia).
In PTL compared to PNL, PGHS-2 was significantly overall increased in all the phenotype specific groups except placental abruption (p < 0.05). PGHS-2 levels were also significantly increased in twin no labour versus PNL (p < 0.05), but there was no difference in PGHS-2 expression between twin no labour and twin labour. There was no statistical difference in the expression of PGHS-2 when the different phenotypes of PTL were compared to both EAL and ESL.
There was no significant change in the expression of CXCL-8 or OTR among both the labouring and non-labouring preterm phenotypes. Connexin-43 expression did not change among the preterm groups.
These data show that PGHS-2 appears to play a significant role in driving the process of preterm labour in all distinct phenotypes (except placental abruption).