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Loss of endometrial plasticity in recurrent pregnancy loss (MeDIP-Seq)

ABSTRACT: Decidual transformation of the human endometrium is not dependent on embryo implantation. Instead, this process is initiated during the mid-luteal phase of each cycle in response to the postovulatory rise in progesterone and increasing endometrial cAMP levels. Consequently, decidualization is a reiterative process directly linked to cyclic activation of mesenchymal stem cells (MSCs) and subsequent differentiation into mature stromal cells in regenerating endometrium. We reasoned that aberrant remodeling of the HESC epigenome would disrupt decidualization in RPL patients and account for the functional memory of HESCs in culture. To explore this possibility, we performed MeDIP-seq, which involves immunoprecipitation of DNA with a 5-methylcytosine antibody followed by deep sequencing, on primary HESC cultures established from four RPL patients and four control subjects. Eight samples were analyzed: derived from four control and four recurrent pregnancy loss (RPL) patient cultures.

ORGANISM(S): Homo sapiens

SUBMITTER: Jan Brosens

PROVIDER: E-GEOD-65100 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Loss of endometrial plasticity in recurrent pregnancy loss (MeDIP-Seq)

Project description:Decidual transformation of the human endometrium is not dependent on embryo implantation. Instead, this process is initiated during the mid-luteal phase of each cycle in response to the postovulatory rise in progesterone and increasing endometrial cAMP levels. Consequently, decidualization is a reiterative process directly linked to cyclic activation of mesenchymal stem cells (MSCs) and subsequent differentiation into mature stromal cells in regenerating endometrium. We reasoned that aberrant remodeling of the HESC epigenome would disrupt decidualization in RPL patients and account for the functional memory of HESCs in culture. To explore this possibility, we performed MeDIP-seq, which involves immunoprecipitation of DNA with a 5-methylcytosine antibody followed by deep sequencing, on primary HESC cultures established from four RPL patients and four control subjects.

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Endometrial protein expression and phosphorylation landscape decipher aberrant insulin and mTOR signaling in patients with recurrent pregnancy loss

Project description:Research question: What are the proteomic and phosphoproteomic differences between the endometrium of women with recurrent pregnancy loss (RPL) and healthy control women during the proliferative (P) and secretory (S) phases of the menstrual cycle? Design: The present study collected a total of 54 endometrial samples during either P or S phases from women with RPL (n = 28) or healthy control (n = 26). Comprehensive proteomic and phosphoproteomic analyses were conducted using label-free liquid chromatography-tandem mass spectrometry (n = 44) and verified through western blotting (n = 10). Three comparison groups were established, including the total RPL endometrium compared to the total control (R/C), proliferating endometrium compared to control (RP/CP), and secretory endometrium compared to control (RS/CS). Results: Differentially expressed proteins (DEPs) and differentially phosphorylated proteins (DPPs) were respectively identified in the three comparison groups. Combining pathway enrichment, network analysis, and soft clustering analysis, we identified the insulin/cyclic nucleotide signaling pathway and AMPK/mTOR signaling pathway as the major contributors to the aberration of RPL endometrium. Western blotting verified altered expression of four proteins, including PRKAR1B, ADCY3, PRKAA2, and LPIN2.Conclusions: This exploratory study provides insights into the differentiated protein expression and phosphorylation profiles of RPL endometrium in both P and S phases. The results highlight potential proteins associated with RPL pathogenesis that may serve as potential indicators for RPL. The findings contribute to the identification of potential targets for RPL treatment as well as the pathogenesis of RPL.

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Single-cell sequencing reveals a delicate molecular and cellular interaction during decidualization in humans

Project description:Proper decidualization is a critical determinant of pregnancy success. Deficiencies in decidualization are associated with a variety of pregnancy disorders, including female infertility, recurrent implantation failure, and miscarriage. However, the mechanism for triggering decidualization of human endometrium is largely unknown. Here we characterized the transcriptomes of four major cells in human endometrium and decidua at single-cell resolution. We discovered the dynamic change characteristics of six major stromal cells. More importantly, a dialogue between IGF1+ stromal cells and IGF1R+ stromal cells initiates endometrial decidualization under regulation of progesterone and estrogen, and IL1B+ stromal cells trigger the apoptosis of epithelial cells and functional remodeling during decidualization. We defined a unique AREG+ NK cell for accelerating decidualization by interacting with IGF1+ stromal cells, and observed that extravillous trophoblasts promote decidualization possibly by multiply pathways. Additionally, we developed a systematic repository of cell-cell communication for decidualization via the ligand-receptor complexes interactions. Our study provides deeper insights into the molecular and cellular characterizations during decidualization.

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Genome-wide Profiling of NR2F2 (COUP-TFII) Binding in Human Endometrial Stromal Cells [ChIP-Seq]

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2015-10-28 | E-GEOD-74373 | biostudies-arrayexpress

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