Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from in vitro decidualized human uterine fibroblast cells (HuF cells) with or without NOTCH1 silencing

ABSTRACT: Decidualization is a critical process for embryo implatation during which uterine stromal fibroblasts are transformed into large, epithelioid-like decidual cell. NOTCH1 is recepotor of Notch signaling that plays important roles for cell-cell communication, which involves gene regulatory mechanisms that control multiple cellular differentiation processes during embryonic and adult life. Here we silenced NOTCH1 by shRNA in HuF cells and studied how it affects decidualization HuF cells were cultured, transfected with NOTCH1 shRNA via a lentivirus system, following by a in vitro induced decidualization by EPC cocktail (36 nM estradiol-17Î² and 1 Î¼M medroxyprogesterone acetate, and 0.1 mM dbcAMP) for 6 days. RNAs were extracted then hybridized on Affymetrix microarrays. There are four experimental conditions: 1) transfected with empty plasmid; 2) transfected with hNOTCH1 lentiviral-shRNA plasmid; 3) transfected with empty plasmid and treated with EPC cocktail; and 4) hNOTCH1 lentiviral-shRNA plasmid with subsequent treatment of EPC cocktail. HuF cells from two different patients were used in each group (HuF86P4 & HuF88P4).

ORGANISM(S): Homo sapiens

SUBMITTER: Renwei Su

PROVIDER: E-GEOD-61827 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Uterine receptivity implies a dialogue between the hormonally primed maternal endometrium and the free-floating blastocyst. Endometrial stromal cells proliferate, avert apoptosis, and undergo decidualization in preparation for implantation; however, the molecular mechanisms that underlie differentiation into the decidual phenotype remain largely undefined. The Notch family of transmembrane receptors transduce extracellular signals responsible for cell survival, cell-to-cell communication, and trans-differentiation, all fundamental processes for decidualization and pregnancy. Using a murine artificial decidualization model, pharmacological inhibition of Notch signaling by gamma-secretase inhibition resulted in significantly decreased deciduoma. Furthermore, a progesterone receptor (PR)-Cre Notch1 bigenic (Notch1d/d) confirmed a Notch1-dependant hypomorphic decidual phenotype. Microarray and pathway analysis, following Notch1 ablation, demonstrated significantly altered signaling repertoire. Concomitantly, hierarchical clustering demonstrated Notch1-dependent differences in gene expression. Uteri deprived of Notch1 signaling demonstrated decreased cellular proliferation; namely, reduced proliferation-specific antigen, Ki67, altered p21, cdk6, and cyclinD activity, and increased apoptotic-profile, augmented cleaved caspase-3, Bad, and attenuated Bcl2. Demonstrated here, the pre-implantation uterus relies on Notch signaling to inhibit apoptosis of stromal fibroblasts and regulate cell cycle progression, which together promotes successful decidualization. In summary, Notch1 signaling modulates multiple signaling mechanisms crucial for decidualization and we provide greater perspective to the coordination of multiple signaling modalities required during decidualization RNA samples from 3-5 separate mice were extracted. All mRNA quantities were normalized against 18S gene expression. Gene expression levels were measured by real-time RT-PCR SYBR Green analysis using the ABI Prism 7700 Sequence Detector System according to manufacturer’s instructions (Applied Biosystems).

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Expression data from in vitro decidualized human uterine fibroblast cells (HuF cells) with or without NOTCH1 silencing

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