ISSN: 2474-9230
Authors: Esma Kirimlioglu, Farida Qulieva, Mehmet Simsek and Necdet Demir*
Spontaneous loss is seen 12-15 % in all pregnancies. More than %50 of those patients do not have a defined etiology, so they are named unexplained Recurrent Pregnancy Loss (URPL). Studies in recent years have made us think that Pregnancy Losses may be related to insufficient decidualization and undetected prothrombotic problems. Tyro3 receptor kinase (RTK) is a member of TAM receptors and has been reported to have an important role in migration, Epithelial-mesenchymal transition (EMT), and platelet aggregation. There is not sufficient knowledge about expression levels of Tyro3 RTK in human first-trimester URPL decidua (URPLD). By immunohistochemistry, immunoblotting, and qPCR, we investigated the expression of Tyro3 RTK in the decidua of human first-trimester termination healthy pregnancy (TPD)(n:6) and URPLD(n:6), and human endometrium (CE)(n:6). Our results suggest that Tyro3 RTK expression significantly decreases with pregnancy and then returns to levels of CE for URPLD. Considering the role of Tyro3 RTK in platelet activation and thrombus formation, it suggests that this decrease observed in TPD may prevent the formation of prothrombosis which can prevent placental flow, and thus, hemostasis could be regulated in pregnancy through Tyro3 RTK. Although Tyro3 RTK decrease in TPD, locally increase on TPD, and also decrease on URPLD of Tyro3 RTK on DSCs makes us think, which Tyro3 RTK has a regulating role for EMT formation on DSCs and may participate in implantation and survival processing of the embryo through DSCs. If those predictions are supported by further functional analyses, one of the causes of URPLD can be enlightened.
Keywords: Unexplained Recurrent Pregnancy Loss; Tyro3 Receptor Kinase; Decidual Stromal Cell; Pregnancy
