E-GEOD-46890
Ontology highlight
ABSTRACT:
PROVIDER: E-GEOD-46890 | ExpressionAtlas | 2015-07-13
REPOSITORIES: ExpressionAtlas
Similar Datasets
Project description:GENE EXPRESSION PROFILE REGULATED BY THE HPV16-E7 ONCOPROTEIN AND ESTRADIOL IN CERVICAL TISSUE
| PRJNA202934 | ENA
Project description:Scarcity of gender specific donor hearts highlights the importance of mesenchymal stem cells (MSCs) as a therapeutic tool for heart repair. However, inefficient incorporation, retention, and activity of MSCs in cardiac tissue remains an obstacle. Since surge in follicular estradiol (μmolar-range) triggers tissue remodeling (e.g. ovulation) and estradiol exerts beneficial actions on the cardiovascular system, we hypothesized that estradiol may promote/improve MSC-mediated cardiac repair processes. Methods: Wharton’s jelly-derived MSCs were used, to assess the effects of estradiol on their proliferation, directed-migration and engraftment in murine heart slices, ex vivo. Results: MSCs expressed estrogen receptors (ERs) α and β, and estradiol promoted MSC proliferation (measured using xCELLigence real-time cell-impedance system and DNA-quantification). Estradiol up-regulated mRNA (qRT-PCR) and protein expression (western blotting) of ERα, ERβ, EMMPRIN, and MMP-9, yet down-regulated MMP-2 expression. In MSCs estradiol, up-regulated mRNA expression of VEGF-A, VCAM-1, and angiogenin, and stimulated NO production via ER. Proteomic analysis revealed that in MSCs estradiol up-regulated 47 proteins, down-regulated 7 proteins, and increased the expression of key biochemical components/pathways involved in tissue repair. In MSCs co-cultured with murine heart-slices, estradiol significantly induced MSC migration in an ER-dependent fashion (and preferentially via ERα) and significantly increased the secretion of MMP-2, MMP-9, angiogenin and VEGF. Conclusion: Estradiol facilitates the integration/engraftment of MSCs into heart slices by promoting MSC proliferation and migration and these beneficial effects are mediated via increases in molecules/pathways involved in tissue remodeling and angiogenesis. Priming of MSCs with estradiol may enhance their ability to repair/regenerate cardiac tissue in women.
2019-06-24 | PXD011742 | Pride
Project description:<p>In this study, lymphoblastoid cell line cultures (LCLs) from women with premenstrual dysphoric disorder (PMDD) and asymptomatic controls were compared via whole-transcriptome sequencing (RNA-seq) during untreated (ovarian steroid-free) conditions and after estradiol and progesterone treatment. In untreated LCLs, pathway analysis of the LCL transcriptome revealed, among others, over-expression of ESC/E(Z) complex genes (an ovarian steroid-regulated gene silencing complex) with significant overexpression of MTF2, PHF19, and SIRT1 (P<0.05) in cells from women with PMDD compared with controls. Finally, mRNA expression of several ESC/E(Z) complex genes were increased by progesterone in controls only, and decreased by estradiol in PMDD LCLs. </p>
| phs001344 | dbGaP
Project description:The HPV16-E7 oncoprotein and 17β-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17β-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17β-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17β-estradiol, provides the basis for further studies on their role in cervical carcinogenesis.
2013-07-01 | GSE46890 | GEO
Project description:Primary outcome(s): The clinical significance of immune and gene-expression profile in colorectal cancer
| 2659791 | ecrin-mdr-crc
Project description:Primary outcome(s): Comparison of the gene expression profile in hair follicle between cancer patients and healthy volunteer
| 2628246 | ecrin-mdr-crc
Project description:Non-linear relationship between chromatin accessibility and estradiol-regulated gene expression
| PRJNA604072 | ENA
Project description:The HPV16-E7 oncoprotein and 17β-estradiol are import factors for the induction of premalignant lesions and cervical cancer. The study of these factors is crucial for a better understanding of cervical tumorigenesis. In this study, we performed a microarray analysis to obtain a global gene expression profile induced by both, HPV16-E7 and 17β-estradiol in cervical tissue of K14E7 transgenic mice. We found that 17β-estradiol is the main cause of the up-regulation of a large number of cellular genes involved in the immune response whereas E7 oncoprotein mainly affects the cellular metabolism. Our microarray data also shows some novel differentially expressed genes that were not previously reported in cervical cancer. The identification of these genes, regulated by E7 and 17β-estradiol, provides the basis for further studies on their role in cervical carcinogenesis. 15 Mouse Gene 1.0 ST Affymetrix microarrays were used to analyze gene expression of cervical tissue from K14E7 hemizygote and nontransgenic FvB control virgin female untreated and treated mice. Briefly, one-month virgin female transgenic and nontransgenic mice were implanted in the dorsal skin with continuous release pellets delivering 0.05 mg of17-β estradiol over 60 days. As control samples we used K14E7 and FvB untreated mice. For the microarray analysis we used triplicates for each group (3 treated K14E7 mice, 3 treated FvB mice, 3 untreated K14E7 mice, 3 untreated FvB mice).
2013-07-01 | E-GEOD-46890 | biostudies-arrayexpress
