Balkan Journal of Medical Genetics

INCREASED EXPRESSION OF PENTRAXIN 3 IN PLACENTAL TISSUES FROM PATIENTS WITH UNEXPLAINED RECURRENT PREGNANCY LOSS
Zeybek S1,*, Tepeli E2, Cetin GO3, Caner V3, Senol H4, Yildirim B2, Bagci G3
*Corresponding Author: Selcan Zeybek, M.D., Department of Medical Genetics, Erzurum Regional Training and Research Hospital, Cat Volu Street, 25070, Erzurum, Turkey. Tel.: +90-506-399-2644. Fax: +90-442-232-5025. E-mail: selcankesan@yahoo.com
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DISCUSSION

The multifunctional protein PTX3 is a well-known pattern recognition receptor that interacts with multiple ligands, including C1q, fibroblast growth factor 2, and P-selectin. The PTX3 is also reportedly involved in the pathogenesis of disorders such as atherosclerosis and inflammatory rheumatic disease and in pregnancy-related problems such as preeclampsia and preterm births [16,17]. Several previous studies showed a significant overexpression of PTX3 depending on disease severity in women with preeclampsia [18,19]. Furthermore, when maternal plasma PTX3 levels were measured during the early weeks of pregnancy, subjects who later developed preeclampsia were found to have significantly higher levels than those who did not develop preeclampsia [20-22]. Therefore, PTX3 may be considered an early marker of placental dysfunction. Incorrect decidualization and implantation was previously observed in Ptx3–/– mice, suggesting that PTX3 plays an important role in blastocyst invasion during endometrial differentiation and implantation stages [23]. The PTX3 is one of the few genes that are induced in fetal implantation areas and is expressed most strongly from decidualized stromal cells following inflammatory events that are mediated by trophoblasts, natural killer cells and antigenpresenting cells [24,25]. To the best of our knowledge, the present study is the first to investigate PTX3 mRNA and protein levels in placental tissues from women with URPL using qRT-PCR and IHC. Recent studies indicate that the highest PTX3 levels in plasma occur during labor [13,14,26]. Moreover, significant differences in plasma PTX3 levels were observed between women with differing types of delivery. Specifically, significantly higher PTX3 levels were observed after vaginal deliveries than after cesarean deliveries [27,28]. Therefore, we excised tissue sections containing trophoblast and decidual cells from the maternal side of placenta after full-term healthy pregnancies and excluded women with cesarean deliveries from the control group. In a 2012 publication, Ibrahim et al. [29] demonstrated the relationship between PTX3 levels and recurrent miscarriage. They compared plasma PTX3 concentrations between patients with primary recurrent miscarriages and pregnant women at the same gestational week and found significantly higher plasma PTX3 levels in the miscarriage group and a positive correlation with numbers of previous miscarriages. Herein, we determined PTX3 expression in placental tissues, and similar to previous studies, we observed 116-fold higher PTX3 expression in the patient group than in the control group. We did not, however, observe significant correlations with age, numbers of previous miscarriages, gestational week of the current miscarriage, or the number of previous live births. Nonetheless, PTX3 expression levels differed significantly between patients who had no live births and women with previous live births. We suggest that aberrant inflammatory signaling contributes to URPL and involves PTX3. In agreement with this hypothesis, the PTX3 ligand C1q reportedly plays key roles in trophoblast invasion, spiral artery remodeling, and normal placentation [30,31], and abnormal distributions of C1q have been associated with adverse pregnancy outcomes such as miscarriage, preterm delivery and pre-eclampsia [32]. In the present study, we found that PTX3 expression was dramatically increased in placental tissues from patients with URPL. Hence, immune dysregulation may be among the etiological factors for URPL, but further functional studies are needed to examine the interactions between PTX3 and other immunological signaling molecules that are stimulated under the conditions of URPL.

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