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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Fazleabas, Asgerally T. Strug, Michael R. Miele, Lucio Jeong, Jae-wook Su, Ren-wei |
| Description | Author Affiliation: Su RW ( Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI 49503); Strug MR ( Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI 49503); Jeong JW ( Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI 49503); Miele L ( Department of Genetics, Louisiana State University Health Sciences Center and Stanley S. Scott Cancer Center, New Orleans, LA 70112.); Fazleabas AT ( Department of Obstetrics, Gynecology and Reproductive Biology, Michigan State University, Grand Rapids, MI 49503); |
| Abstract | In mammalian reproduction, implantation is one of the most critical events. Failure of implantation and the subsequent decidualization contribute to more than 75% of pregnancy losses in women. Our laboratory has previously reported that inhibition of Notch signaling results in impaired decidualization in both women and a transgenic mouse model. In this study, we generated a Notch gain-of-function transgenic mouse by conditionally overexpressing the Notch1 intracellular domain (N1ICD) in the reproductive tract driven by a progesterone receptor (Pgr) -Cre. We show that the overexpression of N1ICD in the uterus results in complete infertility as a consequence of multiple developmental and physiological defects, including the absence of uterine glands and dysregulation of progesterone and estrogen signaling by a Recombination Signal Binding Protein Jκ-dependent signaling mechanism. We further show that the inhibition of progesterone signaling is caused by hypermethylation of its receptor Pgr by Notch1 overexpression through the transcription factor PU.1 and DNA methyltransferase 3b (Dnmt3b). We have generated a mouse model to study the consequence of increased Notch signaling in female reproduction and provide the first evidence, to our knowledge, that Notch signaling can regulate epigenetic modification of the Pgr. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 8 |
| Volume Number | 113 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2016-02-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Infertility, Female Etiology Metabolism Receptor, Notch1 Receptors, Progesterone Uterus Animals DNA Methylation Disease Models, Animal Epigenesis, Genetic Estradiol Immunoglobulin J Recombination Signal Sequence-Binding Protein Deficiency Genetics Mice Mice, Knockout Mice, Transgenic Pregnancy Progesterone Promoter Regions, Genetic Protein Structure, Tertiary RNA, Messenger Chemistry Recombinant Proteins Signal Transduction Up-Regulation Pathology Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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