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Genome-wide transcriptional effects of Pregnancy-Induced Non-coding RNA (PINC)

ABSTRACT: Pregnancy-Induced Non-Coding RNA (PINC) is upregulated in alveolar cells of the mammary gland during pregnancy and persist in alveolar cells that remain in the regressed lobules following involution. Here, we show that in the post-pubertal mouse mammary gland, mPINC expression increases throughout pregnancy and then declines in early lactation, when alveolar cells undergo terminal differentiation. Accordingly, mPINC expression is significantly decreased when HC11 mammary epithelial cells are induced to differentiate and produce milk proteins. This natural reduction in mPINC levels may be necessary for lactation, as overexpression of mPINC in HC11 cells blocks lactogenic differentiation, while knockdown of mPINC enhances differentiation. HC11 mammary epithelial cells, with or without knockdown or over-expression of PINC, and with or without treatment by differentiation-inducing agents, were profiled for gene expression.

ORGANISM(S): Mus musculus

SUBMITTER: Chad Creighton

PROVIDER: E-GEOD-38052 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide transcriptional effects of Pregnancy-Induced Non-coding RNA (PINC)

Project description:Pregnancy-Induced Non-Coding RNA (PINC) is upregulated in alveolar cells of the mammary gland during pregnancy and persist in alveolar cells that remain in the regressed lobules following involution. Here, we show that in the post-pubertal mouse mammary gland, mPINC expression increases throughout pregnancy and then declines in early lactation, when alveolar cells undergo terminal differentiation. Accordingly, mPINC expression is significantly decreased when HC11 mammary epithelial cells are induced to differentiate and produce milk proteins. This natural reduction in mPINC levels may be necessary for lactation, as overexpression of mPINC in HC11 cells blocks lactogenic differentiation, while knockdown of mPINC enhances differentiation.

2012-08-09 | GSE38052 | GEO

MKL1-dependent tenascin-C transcription

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Expression data from mammary gland during pregnancy and lactation of CBA/CaH, QSi5 and Advanced Intercross Line (AIL; CBA/CaH X QSi5, the 14th generation)

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Gene expression profiling of mammary epithelial cells isolated from Cuzd1-null and heterozygous mice on day 18 of pregnancy

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2014-01-01 | E-GEOD-30939 | biostudies-arrayexpress

EZH2 controls mammary differentiation independently of its methyltransferase activity through controlling genomic STAT5 access

Project description:Mammary development is characterized by the proliferation and progressive differentiation of alveolar epithelium during pregnancy, culminating in lactation. These processes are largely controlled by hormones through transcription factors. We now explore the contributions of histone methyltransferases, which establish H3K27me3 marks, in the temporally-regulated differentiation of mammary epithelium. Loss of EZH2, but not EZH1, resulted in precocious mammary differentiation, which was facilitated by STAT5 binding to specific target genes and their activation. Mammary stem cells were not compromised in the absence of EZH2. Genome-wide H3K27me3 patterns remained intact in the absence of EZH2. Mammary-specific loci were devoid of H3K27me3 marks in mammary progenitor and mature cells, suggesting no regulatory role for this repressive mark. Lastly, the combined absence of EZH1 and EZH2 inhibited the formation of alveoli. Taken together, EZH2 controls temporally-restricted differentiation of mammary epithelium through H3K27me3-independent mechanisms. mRNA-seq and ChIP-seq in MMTV-Cre (Control), E1-/- (E1KO), E1+/-;E2f/f;control (E1+/-E2KO) and Ezh2f/f;control (E2KO) mammary gland tissues or MECs (purified mammary epithelial cells). H3K27me3 and STAT5 ChIP-seqs in mammary tissues at p13; H3K4me3 ChIP-seq in MECs (mammary epithelial cells) at p13; RNA-seqs at mature virgin (with/without prolactin injection), p13 and p18 mammary tissues.

2013-12-31 | E-GEOD-52016 | biostudies-arrayexpress

Liver X Receptor α Activation Enhances Cholesterol Secretion in Lactating Mammary Epithelium

Project description:We profiled differential gene expression in vivo between pregnant day 14 (secretory differentiation) and lactation day 4 (established secretory activation) using isolated mouse mammary epithelial cells depleted of the mammary adipocytes. Liver-X-Receptors are ligand-dependent transcription factors activated by cholesterol metabolites. These receptors induce a suite of target genes required for de novo synthesis of triglycerides and cholesterol transport in many tissues. Two different isoforms -LXRα and LXRβ- have been well characterized in liver, adipocytes, macrophages and intestinal epithelium among others, but their contribution to cholesterol and fatty acid efflux in the lactating mammary gland is poorly understood. We hypothesize that LXR regulates lipogenesis during milk fat production in lactation. Global mRNA analysis of mouse mammary epithelial cells (MECs) revealed multiple LXR/RXR targets are upregulated sharply at the onset of lactation compared to mid-pregnancy. LXRα is the primary isoform and its protein levels increase throughout lactation in MECs. The LXR agonist GW3965 markedly induced several genes involved in cholesterol transport and lipogenesis and enhanced cytoplasmic lipid droplet accumulation in the HC11 MEC cell line. Importantly, in vivo pharmacological activation of LXR increased the milk cholesterol percentage and induced Srebp1c and Abca7 expression in MECs. Cumulatively, our findings identify LXRα as an important regulator of cholesterol incorporation into the milk through key nodes of de novo lipogenesis, suggesting a potential therapeutic target in women with difficulty initiating lactation.

2019-03-05 | GSE121819 | GEO

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Project description:In this study we have used a murine mammary epithelial cell line (HC11) with stem cell characteristics and made a thorough investigation of global gene-expression changes during mammary stem cell differentiation.

2009-09-18 | E-MEXP-1809 | biostudies-arrayexpress

Gene expression profiling of mammary epithelial cells isolated from Cuzd1-null and heterozygous mice on day 18 of pregnancy

2014-01-01 | GSE30939 | GEO

Identification of Ovol2 binding regions in HC11 cells

Project description:Epithelial cells possess remarkable plasticity, having the ability to become mesenchymal cells through alterations in adhesion and motility (epithelial-to-mesenchymal transition or EMT). Recent studies suggest that EMT endows differentiated epithelial cells with stem cell traits, posing the interesting question of how epithelial plasticity is properly restricted to ensure epithelial differentiation during tissue morphogenesis. Here we identify zinc-finger transcription factor Ovol2 as a key suppressor of EMT of mammary epithelial cells. Epithelia-specific deletion of Ovol2 completely arrests mammary ductal morphogenesis, and depletes epithelial stem/progenitor cell reservoirs. Further, Ovol2-deficient epithelial cells undergo EMT in vivo to become non-epithelial cell types, and that Ovol2 directly represses key EMT inducers such as Zeb1 and regulates stem/progenitor cell responsiveness to TGF-beta. We also provide evidence for a suppressive role of Ovol2 in breast cancer progression. Our findings underscore the critical importance of exquisitely regulating epithelial plasticity to balance stemness with epithelial differentiation in development and cancer. We report ChIPseq data illustrating Ovol2 genome-wide targets in mouse mammary epithelial cells, suggesting that Ovol2 regulates a plethora of genes associated with the EMT process. Immunoprecipitated samples from HC11 mouse mammary epithelial cells with antibodies against Ovol2 and control IgG respectively were used for ChIP-seq experiments.

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