Ozer Erdener
Department of Pathology, Dokuz Eylul University School of Medicine, Izmir, Turkey.
Pediatr Dev Pathol. 2008 Sep-Oct;11(5):344-9. doi: 10.2350/07-10-0361.1. Epub 2008 Feb 8.
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.
胎膜早破（PROM）是一种与早产相关的并发症。由于大多数新生儿死亡、发病及费用都与早产有关，因此了解早产胎膜早破（pPROM）的发病机制至关重要。本研究的目的是调查绒毛膜滋养层细胞的端粒酶活性是否在PROM的发病机制中起作用。收集了56例pPROM患者和45例早产（PTL）患者的胎盘胎膜。通过免疫组织化学评估端粒酶活性，并计算两组的端粒酶活性指数（TAI）。结果以平均值±标准差表示。采用独立样本t检验分析组间差异。为评估其他可能的机制，如细胞凋亡和细胞外基质降解，还进行了基质金属蛋白酶（MMP）-9、金属蛋白酶组织抑制剂（TIMP）-3和M30 CytoDEATH抗体的免疫组织化学检测。PTL组的TAI为6.8±3.2，而pPROM组为2.5±1.5。与PTL相比，pPROM胎膜中的TAI降低具有统计学意义（P<0.001）。pPROM胎膜的凋亡滋养层细胞数量显著增加（P<0.001），而两组的绒毛膜滋养层细胞以及其他细胞中均发现MMP-9和TIMP-3染色较强。虽然对pPROM的研究主要集中在导致胎膜程序性弱化过程的基质金属蛋白酶激活和细胞凋亡上，但绒毛膜滋养层细胞端粒酶活性降低可能在pPROM的发病机制中也起一定作用。
