Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA183647 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Progesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used microarray analysis to identify global gene expression signatures that are acutely regulated by PRs in the mouse mammary gland after acute P treatment. Mammary gland gene expression data from 10-week-old ovariectomized wildtype and progesterone receptor null mice treated subcutaneously with 17β-Estradiol for 24 hours and then 17β-Estradiol plus Progesterone for 8 or 24 hours. Three replicate pools were tested with three mice per pool.
2013-08-27 | E-GEOD-42858 | biostudies-arrayexpress
Project description:Beyond demonstrating a critical role for progesterone receptor signaling in normal mammary epithelial proliferation, the progesterone receptor knockout mouse disclosed the progesterone receptor along with its effector pathways as key determinants of mammary neoplastic progression. Despite these advances, however, further progress in our mechanistic understanding of progesteroneâ??s involvement in mammary morphogenesis and tumorigenesis is contingent upon defining the essential effector pathways responsible for transducing the progesterone signal into a mammary proliferative and/or pro-survival response. Toward this goal, a judiciously chosen acute progesterone treatment regimen together with microarray methods was applied to the mammary gland of the normal mouse to uncover new effectors that operate immediately downstream of the progesterone mammary signal. Examination of the resultant progesterone-responsive transcriptome disclosed â??inhibitor of differentiation or DNA binding 4â?? (Id4) as a molecular target acutely induced by progesterone in the murine mammary epithelium. Experiment Overall Design: Microarray analysis was performed on mammary tissue total RNA obtained from ovariectomized mice previously treated with progesterone for 4, 16, 28, and 76 hours. For each hormone treatment time-point, mammary gland microarray data from sesame oil (vehicle) treated mice was included as controls. Total mammary gland RNA from each time-point and treatment group was interrogated using the Affymetrix GeneChip Mouse Genome 430 2.0 Array. For a given time-point and treatment group, three sets of mice (5 mice in each set) were used for gene expression profiling; mammary RNA pooled from each set was hybridized to one microarray chip. Therefore, a total of 15 mice (or 3 microarray chips) were used per time-point and treatment group.
2008-11-22 | E-GEOD-10290 | biostudies-arrayexpress
Project description:Beyond demonstrating a critical role for progesterone receptor signaling in normal mammary epithelial proliferation, the progesterone receptor knockout mouse disclosed the progesterone receptor along with its effector pathways as key determinants of mammary neoplastic progression. Despite these advances, however, further progress in our mechanistic understanding of progesterone’s involvement in mammary morphogenesis and tumorigenesis is contingent upon defining the essential effector pathways responsible for transducing the progesterone signal into a mammary proliferative and/or pro-survival response. Toward this goal, a judiciously chosen acute progesterone treatment regimen together with microarray methods was applied to the mammary gland of the normal mouse to uncover new effectors that operate immediately downstream of the progesterone mammary signal. Examination of the resultant progesterone-responsive transcriptome disclosed “inhibitor of differentiation or DNA binding 4” (Id4) as a molecular target acutely induced by progesterone in the murine mammary epithelium. Keywords: time course
2008-11-15 | GSE10290 | GEO
Project description:Progesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used microarray analysis to identify global gene expression signatures that are acutely regulated by PRs in the mouse mammary gland after acute P treatment.
2013-08-27 | GSE42858 | GEO
Project description:Progesterone receptor ChIP-seq within the mouse mammary gland
| PRJNA183705 | ENA
Project description:Progesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) to identify P-regulated genes that directly recruit PRs in the mouse mammary gland after acute P treatment. Two replicate PR ChIP samples and two replicate input DNA control samples from mouse mammary glands after mice are treated subcutaneously with 17?-Estradiol for 24 hours and then 17?-Estradiol plus Progesterone for 6 hours.
2013-08-27 | E-GEOD-42887 | biostudies-arrayexpress
Project description:Estrogen receptor α (ERα) is the major driving transcription factor in normal mammary gland development as well as breast cancer initiation and progression.However,the fundamental mechanisms,including global cistromic and genomic transcriptional responses that are required to elicit mammary epithelial cell proliferation in response to estradiol, have not been elucidated. We used RNA-seq analysis to identify global gene expression signatures that are acutely regulated by estroegn receptors in the mouse mammary gland after acute estradiol treatment.
2019-07-23 | GSE130031 | GEO
Project description:Progesterone (P) acting through its cognate nuclear receptors (PRs) plays an essential role in driving pregnancy-associated branching morphogenesis of the mammary gland. However, the fundamental mechanisms, including global cistromic and acute genomic transcriptional responses that are required to elicit active branching morphogenesis in response to P, have not been elucidated. We used chromatin immunoprecipitation followed by deep sequencing (ChIP-seq) to identify P-regulated genes that directly recruit PRs in the mouse mammary gland after acute P treatment.
2013-08-27 | GSE42887 | GEO
Project description:Clinical studies have linked use of progestins (synthetic progesterone (P4)) to breast cancer risk. However, little is understood regarding the role native P4, signaling through the progesterone receptor (PR), plays in formation of breast tumors. Studies published by our lab highlighted a link between PR and immune signaling pathways, suggesting PR induces PR to repress the interferon signaling pathway. Given these findings, we sought to investigate whether P4/PR drive immunomodulation in the mammary gland and development of mammary gland tumors. We found that mice treated with P4 displayed changes in the mammary gland suggesting inhibited immune response compared to placebo-treated mice. Furthermore, transgenic mice with PR overexpression demonstrated decreased numbers of immune cell populations in their mammary gland, lymph nodes, and spleens. Upon long-term monitoring, we determined that multi-parous PR overexpressing mice developed significantly more mammary gland tumors than control mice. Additionally, tumors of PR overexpressing mice contained fewer infiltrating immune cells. Finally, RNA sequencing analysis of tumor samples revealed that immune-related gene signatures were enriched in tumors of control mice compared to tumors of PR overexpressing mice. Together, these findings provide a novel mechanism behind P4-mediated promotion of mammary gland tumor development and provide rationale to investigate anti-progestin treatment to promote immune-mediated elimination of mammary gland tumors.
2021-09-15 | GSE158134 | GEO
Project description:Estrogen receptor-depended gene signatures in the mouse mammary gland after acute estradiol treatment (RNA-Seq)
| PRJNA533618 | ENA