Telomerase activity of chorionic trophoblasts in preterm premature rupture of membranes.

Premature rupture of membranes (PROM) is a complication associated with preterm birth. Because most neonatal death, morbidity, and cost are linked to preterm birth, understanding the mechanisms for developing preterm PROM (pPROM) is critical. The aim of this study is to investigate whether telomerase activity of the chorionic trophoblasts may play a role in the pathogenesis of PROM. Placental membranes were collected from 56 patients with pPROM and 45 patients with preterm labor (PTL). Telomerase activity was assessed by immunohistochemistry, and telomerase activity index (TAI) was calculated for both groups. Results are expressed as the mean +/- standard deviation. Differences between groups were analyzed using an independent-samples t-test. To evaluate other suggested mechanisms, such as apoptosis and extracellular matrix degradation, immunohistochemistry for matrix metalloproteinase (MMP)-9, tissue inhibitor of metalloproteinase (TIMP)-3, and M30 CytoDEATH antibodies were also performed. The TAI was found to be 6.8 +/- 3.2 for PTL, while it was 2.5 +/- 1.5 for pPROM. Decreased TAI was statistically significant in pPROM membranes in comparison with PTL (P < 0.001). Number of apoptotic trophoblasts was significantly increased for the membranes of pPROM (P < 0.001), whereas strong staining of MMP-9 and TIMP-3 was found for chorionic trophoblasts as well as for other cells in both groups. Although study of the pPROM has focused on activation of matrix metalloproteinases and apoptosis that result in the consequence of a programmed membrane weakening process, decreased telomerase activity of chorionic trophoblasts is likely to have a contributing role in the pathogenesis of pPROM as well.