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Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE54150 | GEO | 2015/01/22

SECONDARY ACCESSION(S): PRJNA235304

REPOSITORIES: GEO

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Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-01-22 | E-GEOD-54150 | biostudies-arrayexpress

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [mRRBS]

Project description:Mammary gland development and luminal differentiation occur largely postnatally during puberty and pregnancy. We found that pregnancy had the most significant effects on stem cells, inducing a distinct epigenetic state that remained stable through life. Mammary glands were collected from mice at non-pregnant and pregnant stages for DNA extraction and DNA methylation analysis via mRRBS (multiplexed reduced representation bisulfite sequencing).

2015-01-22 | E-GEOD-54149 | biostudies-arrayexpress

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [mRRBS]

2015-01-22 | GSE54149 | GEO

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [reproductive stages]

Project description:Mammary gland development and luminal differentiation occur largely postnatally during puberty and pregnancy. We found that pregnancy had the most significant effects on stem cells, inducing a distinct epigenetic state that remained stable through life. Mammary glands were collected from different reproductive stages to purify different epithelium cell types, which were used for RNA extraction and hybridization on Affymetrix microarrays.

2015-01-22 | E-GEOD-54147 | biostudies-arrayexpress

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [inhibitor study]

Project description:Mammary gland development and luminal differentiation occur largely postnatally during puberty and pregnancy. To explore the role of DNA methylation in luminal cell differentiation and pregnancy-induced changes, we determined the genome-wide DNA methylation and gene expression profiles of mammary epithelial stem, luminal progenitor, and mature luminal cells at different reproductive stages. We found that pregnancy had the most significant effects on stem cells, inducing a distinct epigenetic state that remained stable through life. Integrated analysis of gene expression, DNA methylation, and histone modification profiles revealed cell type and reproductive stage-specific changes in molecular signatures. We also identified p27 and TGFβ signaling as key regulators of luminal progenitor cell proliferation based on their expression patterns and by the use of explant cultures. Our results suggest relatively minor changes in DNA methylation during luminal cell differentiation as compared to the significant effects of pregnancy on mammary epithelial stem cells. Mammary glands were collected from mice treated with DNA methylation inhibitor 5-azacytidine (AzaC) and histone deacetylase inhibitor valproic acid (VPA) at non-pregnant and pregnant stages for RNA extraction and hybridization on Affymetrix microarrays.

2015-01-22 | E-GEOD-54148 | biostudies-arrayexpress

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [inhibitor study]

2015-01-22 | GSE54148 | GEO

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells [reproductive stages]

2015-01-22 | GSE54147 | GEO

Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells

Project description:Pregnancy-associated alterations in DNA methylation patterns of mammary epithelial stem cells

| PRJNA235304 | ENA

Age- and pregnancy-associated DNA methylation changes in mammary epithelial cells.

Project description:Postnatal mammary gland development and differentiation occur during puberty and pregnancy. To explore the role of DNA methylation in these processes, we determined the genome-wide DNA methylation and gene expression profiles of CD24(+)CD61(+)CD29(hi), CD24(+)CD61(+)CD29(lo), and CD24(+)CD61(-)CD29(lo) cell populations that were previously associated with distinct biological properties at different ages and reproductive stages. We found that pregnancy had the most significant effects on CD24(+)CD61(+)CD29(hi) and CD24(+)CD61(+)CD29(lo) cells, inducing distinct epigenetic states that were maintained through life. Integrated analysis of gene expression, DNA methylation, and histone modification profiles revealed cell-type- and reproductive-stage-specific changes. We identified p27 and TGFβ signaling as key regulators of CD24(+)CD61(+)CD29(lo) cell proliferation, based on their expression patterns and results from mammary gland explant cultures. Our results suggest that relatively minor changes in DNA methylation occur during luminal differentiation compared with the effects of pregnancy on CD24(+)CD61(+)CD29(hi) and CD24(+)CD61(+)CD29(lo) cells.

| S-EPMC4325231 | biostudies-literature

TRAF6 maintains mammary stem cells and promotes pregnancy-induced mammary epithelial cell expansion.

Project description:Receptor activator of nuclear factor (NF)-κB (RANK) signaling promotes pregnancy-dependent epithelial cell differentiation and expansion for mammary gland development, which requires NF-κB pathway-dependent Cyclin D1 induction and inhibitor of DNA binding 2 (Id2) pathway-dependent anti-apoptotic gene induction. However, the roles of tumor necrosis factor receptor-associated factor 6 (TRAF6) remain unclear despite its requirement in RANK signaling. Here we show that TRAF6 is crucial for both mammary stem cell maintenance and pregnancy-induced epithelial cell expansion. TRAF6 deficiency impairs phosphoinositide 3-kinase (PI3K)/AKT and canonical NF-κB pathways, whereas noncanonical NF-κB signaling remains functional. Therefore, we propose that TRAF6 promotes cell proliferation by activating PI3K/AKT signaling to induce retinoblastoma phosphorylation in concert with noncanonical NF-κB pathway-dependent Cyclin D1 induction. Furthermore, TRAF6 inhibits apoptosis by activating canonical NF-κB signaling to induce anti-apoptotic genes with the Id2 pathway. Therefore, proper orchestration of TRAF6-dependent and -independent RANK signals likely establishes mammary gland formation.

| S-EPMC6684589 | biostudies-literature

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