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
page: 21

INTRODUCTION

According to the American College of Obstetricians and Gynecologists [1], recurrent pregnancy loss is a disease, defined as two or more failed pregnancies. Recurrent pregnancy loss is one of the most frustrating and difficult areas of reproductive medicine because up to 50.0% of cases lack clearly defined etiology [2]. Common conditions that have been associated with recurrent pregnancy losses include uterine abnormalities, parental chromosomal aberrations, various endocrine disturbances and the presence of antiphospholipid antibodies [3,4]. Uncontrolled inflammatory response is thought an important mechanism underlying development of pregnancy complications such as unexplained pregnancy loss, preeclampsia, fetal growth restriction and death [5,6]. In the placenta, innate and adaptive immune responses influence the balance between anti- and pro-inflammatory decidual environments. These inflammatory changes are essential to various processes that are required for successful embryonic implantation, such as trophoblast invasion, angiogenesis and placental growth [7]. Pentraxins are a superfamily of evolutionarily conserved multifunctional pattern-recognition proteins that play roles in innate humoral immunity. Serum amyloid P component and C reactive protein constitute the short arm of the pentraxin superfamily. Pentraxin 3 (PTX3) is a prototype member of long arm that contains an additional N-terminal domain. Unlike classic pentraxins made in the liver, PTX3 is produced locally by a number of different cells such as mononuclear cells, dendritic cells and endothelial cells [8]. Pentraxin 3 is a multifunctional protein that interacts with various ligands, including elements of the complement system such as C1q, factor H, C4 binding protein, ficolins and mannose-binding lectin; growth factors such as fibroblast growth factor 2; adhesion molecules such as P-selectin; extracellular matrix components such as inter-α-trypsin inhibitor; tumor necrosis factor-inducible gene-6 and fibrin; apoptotic cells, and pathogens such as Klebsiella pneumoniae and Aspergillus fumigatus [9]. Hence, PTX3 plays important roles in innate immunity, complement activation, inflammation, matrix deposition, angiogenesis, vascular remodeling, platelet activation, antimicrobial resistance and tissue repair [8]. Pentraxin 3 also behaves as an acute-phase response protein that is rapidly induced from low blood levels in response to inflammation. Pentraxin 3 expression levels have also been correlated with disease severity under conditions of sepsis, acute myocardial infarction, atherosclerosis, autoimmune disorders and preeclampsia [10,11]. During pregnancy, PTX3 is expressed in amniotic epithelial, chorionic mesoderm, terminal villous trophoblast and placental perivascular stromal tissues, and is increasingly expressed during pregnancy and peaks during labor [12,13]. However, no previous studies have shown PTX3 expression patterns in placental tissues of patients with unexplained recurrent pregnancy loss (URPL). Herein, we determined PTX3 expression levels in patients with URPL and compared these with those in a control group of subjects with a history of healthy live births.



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