Plasma from women with preeclampsia inhibits trophoblast invasion.

نویسندگان

  • L K Harris
  • O H Clancy
  • J E Myers
  • P N Baker
چکیده

To assess whether plasma from women with preeclampsia altered trophoblast invasion, SGHPL-4 extravillous trophoblasts were treated with pooled plasma from women with preeclampsia (PE-P; 10%) or with plasma from healthy pregnant controls (C-P). PE-P significantly inhibited SGHPL-4 invasion through Matrigel-coated transwells (P < .01), reduced mitochondrial dehydrogenase activity (P < .01), and increased apoptosis (P < .05); however, invading cells were no more susceptible to PE-P-induced apoptosis than their static counterparts. C-P did not alter rates of invasion, proliferation, or apoptosis. The bioactivity of PE-P was retained after removal of the 6 most abundant plasma proteins using an immunodepletion column (P < .05). Fractionation of PE-P demonstrated that the reduction in invasion was predominantly mediated by factors >100 kd in size. The authors conclude that plasma from women with preeclampsia contains multiple factors that inhibit invasion. These factors do not specifically target invading cells, but instead may reduce the number of cells available to invade.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Inconformity of CXCL3 Plasma Level and Placenta Expression in Preeclampsia and Its Effect on Trophoblast Viability and Invasion

As a member of the chemokine family, CXCL3 was previously known to participate in many pathophysiological events. However, whether CXCL3 stimulates trophoblast invasion as a key process of preeclampsia pathogenesis remains largely unknown. Therefore, the aim of this study was to investigate this hypothesis and determine the effect of CXCL3 on the first trimester trophoblast. Seventy gravidas we...

متن کامل

Role of nuclear receptors and their ligands in human trophoblast invasion.

Human implantation involves a major invasion of the uterine wall and complete remodelling of uterine arteries by extravillous cytotrophoblasts (EVCT). Abnormality in these early steps of placental development leads to poor placentation, fetal growth defects and is often associated with preeclampsia, a major and frequent complication of human pregnancy. To study the mechanisms that control troph...

متن کامل

A Role for Nrf2 in Redox Signalling of the Invasive Extravillous Trophoblast in Severe Early Onset IUGR Associated with Preeclampsia

BACKGROUND Preeclampsia (PE) is characterized by increased lipid oxidation and diminished antioxidant capacity, while intrauterine growth restriction (IUGR) is characterized by impaired invasion of the extravillous trophoblast. Vascular endothelial growth factor (VEGF) has been reported to be altered in preeclampsia. A relationship between VEGF and nuclear factor erythroid 2-related factor-2 (N...

متن کامل

Long non-coding RNA RPAIN regulates the invasion and apoptosis of trophoblast cell lines via complement protein C1q

Long non-coding RNAs (lncRNAs) are key regulatory molecules that are involved in a variety of biological processes and human diseases. Their impact on early onset preeclampsia remains unclear. In this study, we tested the expression of RPAIN (transcript variant 12 of RPA interacting protein, a non-coding RNA, NR_027683.1) in placenta tissues derived from 25 pregnant women with PE and 15 healthy...

متن کامل

Upregulated unique long 16 binding protein 1 detected in preeclamptic placenta affects human extravillous trophoblast cell line (HTR-8/SVneo) invasion by modulating the function of uterine natural killer cells

Well-controlled trophoblast invasion at the maternal-fetal interface is crucial for normal placentation and successful pregnancy, otherwise pathological conditions of pregnancy occur, such as preeclampsia. In previous studies, it has been demonstrated that unique long 16 binding protein (ULBP)1, a ligand for the natural-killer group (NKG)2D receptor on uterine natural killer (uNK) cells, is upr...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Reproductive sciences

دوره 16 11  شماره 

صفحات  -

تاریخ انتشار 2009