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12. Reversal of gene dysregulation in cultured cytotrophoblasts reveals possible causes of preeclampsia

Author

Zhou, Yan, Gormley, Matthew J, Hunkapiller, Nathan M, Kapidzic, Mirhan, Stolyarov, Yana, Feng, Victoria, Nishida, Masakazu, Drake, Penelope M, Bianco, Katherine, Wang, Fei, McMaster, Michael T, and Fisher, Susan J

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Perinatal Period - Conditions Originating in Perinatal Period, Hypertension, Contraception/Reproduction, Clinical Research, Cardiovascular, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Reproductive health and childbirth, Good Health and Well Being, Animals, COS Cells, Cell Differentiation, Cell Movement, Chick Embryo, Chlorocebus aethiops, Class Ia Phosphatidylinositol 3-Kinase, Female, Gene Expression Regulation, Glycogen Synthase Kinase 3, Humans, Membrane Glycoproteins, Neovascularization, Pathologic, Neuropilin-1, Neuropilin-2, Oligonucleotide Array Sequence Analysis, Placenta, Pre-Eclampsia, Pregnancy, Proto-Oncogene Proteins c-akt, RNA, Messenger, Semaphorins, Signal Transduction, Transcriptome, Trophoblasts, Vascular Endothelial Growth Factor A, beta Catenin, Medical and Health Sciences, Immunology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4%-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) and, in some patients, fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously, we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, we cultured CTBs isolated from PE and control placentas for 48 hours, enabling differentiation and invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation, including upregulation of SEMA3B, which resolved in culture. The addition of SEMA3B to normal CTBs inhibited invasion and recreated aspects of the PE phenotype. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression; the autocrine actions of the upregulated molecules (including SEMA3B) impair CTB differentiation, invasion and signaling; and patient-specific factors determine the signs.

Published
2013

49. Application of the nuclear factor-[kappa]B inhibitor BAY 11-7085 for the treatment of endometriosis: an in vitro study

Author

Nasu, Kaei, Nishida, Masakazu, Ueda, Tami, Yuge, Akitoshi, Takai, Noriyuki, and Narahara, Hisashi

Subjects
Endometriosis -- Research, Cellular control mechanisms -- Research, Apoptosis -- Research, Genetic regulation -- Research, Enzyme inhibitors -- Research, Cell research, Biological sciences
Abstract

Most of the current medical treatments for endometriosis aim to downregulate estrogen activity. However, a high recurrence rate after medical treatment has been the most significant problem. BAY 11-7085, a soluble inhibitor of NK-[kappa]B activation, has been shown to inhibit cell proliferation and induce apoptosis of a variety of cells. To examine the potential application of BAY 11-7085 in the treatment of endometriosis, we investigated the effects of this agent on the cell proliferation and apoptosis of cultured ovarian endometriotic cyst stromal cells (ECSCs) by a modified methylthiazole tetrazolium assay, a 5-bromo-2'-deoxyuridine incorporation assay, and internucleosomal DNA fragmentation assays. The effect of BAY 11-7085 on the cell cycle of ECSCs was also determined by flow cytometry. The expression of apoptosis-related molecules was examined in ECSCs with Western blot analysis. BAY 11-7085 significantly inhibited the cell proliferation and DNA synthesis of ECSCs and induced apoptosis and the G0/G1 phase cell cycle arrest of these cells. Additionally, downregulation of the B-cell lymphoma/leukemia-2 (Bcl-2) and Bcl-[X.sub.L] expression with simultaneous activation of caspase-3, -8, and -9 was observed in ECSCs after treatment with BAY 11-7085. These results suggest that BAY 11-7085 induces apoptosis of ECSCs by suppressing antiapoptotic proteins, and that caspase-3-, -8-, and -9-mediated cascades are involved in this mechanism. Therefore, BAY 11-7085 could be used as a therapeutic agent for the treatment of endometriosis. apoptosis; cell cycle arrest; Bcl-2; Bcl-[X.sub.L] doi:10.1152/ajpendo.00135.2006

Published
2007

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