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
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.

Number 25 VOL. 25(2), 2022	Number 25 VOL. 25 (1), 2022
Number 24 VOL. 24(2), 2021	Number 24 VOL. 24(1), 2021
Number 23 VOL. 23(2), 2020	Number 22 VOL. 22(2), 2019
Number 22 VOL. 22(1), 2019	Number 22 VOL. 22, 2019 Supplement
Number 21 VOL. 21(2), 2018	Number 21 VOL. 21 (1), 2018
Number 21 VOL. 21, 2018 Supplement	Number 20 VOL. 20 (2), 2017
Number 20 VOL. 20 (1), 2017	Number 19 VOL. 19 (2), 2016
Number 19 VOL. 19 (1), 2016	Number 18 VOL. 18 (2), 2015
Number 18 VOL. 18 (1), 2015	Number 17 VOL. 17 (2), 2014
Number 17 VOL. 17 (1), 2014	Number 16 VOL. 16 (2), 2013
Number 16 VOL. 16 (1), 2013	Number 15 VOL. 15 (2), 2012
Number 15 VOL. 15, 2012 Supplement	Number 15 Vol. 15 (1), 2012
Number 14 14 - Vol. 14 (2), 2011	Number 14 The 9th Balkan Congress of Medical Genetics
Number 14 14 - Vol. 14 (1), 2011	Number 13 Vol. 13 (2), 2010
Number 13 Vol.13 (1), 2010	Number 12 Vol.12 (2), 2009
Number 12 Vol.12 (1), 2009	Number 11 Vol.11 (2),2008
Number 11 Vol.11 (1),2008	Number 10 Vol.10 (2), 2007
Number 10 10 (1),2007	Number 9 1&2, 2006
Number 9 3&4, 2006	Number 8 1&2, 2005
Number 8 3&4, 2004	Number 7 1&2, 2004
Number 6 3&4, 2003	Number 6 1&2, 2003
Number 5 3&4, 2002	Number 5 1&2, 2002
Number 4 Vol.3 (4), 2000	Number 4 Vol.2 (4), 1999
Number 4 Vol.1 (4), 1998	Number 4 3&4, 2001
Number 4 1&2, 2001	Number 3 Vol.3 (3), 2000
Number 3 Vol.2 (3), 1999	Number 3 Vol.1 (3), 1998
Number 2 Vol.3(2), 2000	Number 2 Vol.1 (2), 1998
Number 2 Vol.2 (2), 1999	Number 1 Vol.3 (1), 2000
Number 1 Vol.2 (1), 1999	Number 1 Vol.1 (1), 1998

About the journal ::: Editorial ::: Subscription ::: Information for authors ::: Contact