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Gene expression profiling reveals that ERα controls the mitochondrial biogenesis in LysM-Cre targeted cells

ABSTRACT: Estrogens decrease osteoclast numbers via direct and indirect effects. In trabecular bone, the anti-osteoporotic efficacy of estrogens is mediated via the estrogen receptor α (ERα) present in myeloid lineage cells, but the molecular mechanism mediating these effects remain controversial. In contrast to published findings by others, FasLgld/gld mice which lack functional FasL lost cortical and cancellous bone following OVX indistinguishably from FasL-intact controls. Microarray analysis of osteoclast progenitors isolated from the bone marrow of ERαf/f;LysM-Cre mice and ERαf/f controls indicated that ERα deleted macrophages exhibited significant enrichment for the term “oxidative phosphorylation”, suggesting that estrogen signaling via ERα inhibits this process

ORGANISM(S): Mus musculus

PROVIDER: GSE111237 | GEO | 2020/02/14

REPOSITORIES: GEO

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Expression data from Dmp1-GFP sorted osteocytes

Project description:Estrogens are well known steroid hormones necessary to maintain bone health. In addition, mechanical loading, which estrogen signaling may intersect with the Wnt/β-catenin pathway, is also essential for bone health. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ERα deletion mice (ERαΔOcy/ΔOcy) were generated by mating ERα floxed mice with Dmp1-Cre mice to determine functions of ERα in osteocytes. Trabecular bone mineral density of female, but not male ERαΔOcy/ΔOcy mice was significantly decreased. Bone formation parameters in ERαΔOcy/ΔOcy were significantly decreased while osteoclast parameters were unchanged. This suggests that ERα in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ERα, gene array analysis of Dmp1-GFP osteocytes FACS sorted from ERαΔOcy/ΔOcy and control mice was performed. Expression of Mdk and Sostdc1, both known inhibitors of Wnt, were significantly increased without alteration of the mature osteocyte marker Sost or β-catenin. Hindlimb unloading exacerbated the trabecular bone loss, but surprisingly cortical bone was resistant. These studies show that ERα in osteocytes has osteoprotective effects in trabecular bone through regulating expression of Wnt antagonists, but conversely plays a negative role in cortical bone loss due to unloading.

2013-12-12 | GSE41997 | GEO

Osteoclastic estrogen receptor alpha mediates the osteoprotective estrogen action through Fas ligand signaling

Project description:Estrogen clearly prevents osteoporotic bone loss by attenuating bone resorption. The molecular basis of how this is accomplished, however, remains elusive. Here we report a critical role of osteoclastic ERa in mediating estrogen action on bone in females. We selectively ablated ERa in differentiated osteoclasts (ERa dOc/dOc). ERa dOc/dOc females, but not males, exhibited clear trabecular bone loss, similar to the osteoporotic bone phenotype in post-menopausal women. Recovery of bone loss by estrogen treatment of the ovariectomized ERa dOc/dOc females was ineffective in the trabecular areas of the long bones and lumbar vertebral bodies. Osteoclastic apoptosis, induced by estrogen, occurred simultaneously with up-regulation of Fas ligand (FasL) expression in intact trabecular bones of ERa +/+mice, but not in ERa dOc/dOc mice. ERa was also required for similar effects of estrogen and tamoxifen in cultured osteoclasts. These findings suggest that the osteoprotective actions of estrogen and SERMS are mediated at least in part through osteoclastic ERa in trabecular bone; and the life span of mature osteoclasts is regulated through activation of the Fas/FasL system. Keywords: Study about estrogen response of osteoclast-specific estrogen receptor alpha mice

2007-06-01 | GSE7798 | GEO

Transcription profiling of mouse ERa abalated differentiated osteoclasts

Project description:Estrogen clearly prevents osteoporotic bone loss by attenuating bone resorption. The molecular basis of how this is accomplished, however, remains elusive. Here we report a critical role of osteoclastic ERa in mediating estrogen action on bone in females. We selectively ablated ERa in differentiated osteoclasts (ERa dOc/dOc). ERa dOc/dOc females, but not males, exhibited clear trabecular bone loss, similar to the osteoporotic bone phenotype in post-menopausal women. Recovery of bone loss by estrogen treatment of the ovariectomized ERa dOc/dOc females was ineffective in the trabecular areas of the long bones and lumbar vertebral bodies. Osteoclastic apoptosis, induced by estrogen, occurred simultaneously with up-regulation of Fas ligand (FasL) expression in intact trabecular bones of ERa +/+mice, but not in ERa dOc/dOc mice. ERa was also required for similar effects of estrogen and tamoxifen in cultured osteoclasts. These findings suggest that the osteoprotective actions of estrogen and SERMS are mediated at least in part through osteoclastic ERa in trabecular bone; and the life span of mature osteoclasts is regulated through activation of the Fas/FasL system. Experiment Overall Design: Wild type and osteoclast-specific Estrogen Receptor alpha knock-out mice were ovariectomized. The number of both genotypes of mice was eight. The mice of each genotypes were divided to vehicle control and estrogen treated group. Four hours after chemical treatment, the distal 5 mm of the left femurs were harvested after sacrificing by cervical dislocation and total RNAs were purified for Affymetix GeneChip microarray analysis without pooling. Therefore, this experiment consists of four groups with four replicates per group.

2008-06-15 | E-GEOD-7798 | biostudies-arrayexpress

The estrogen receptor α is required and sufficient to maintain physiological glucose uptake in the mouse heart

Project description:Rationale: Estrogens attenuate cardiac hypertrophy and increase cardiac contractility via their cognate receptors ERα and ERβ. Since female sex hormones enhance global glucose utilization and because myocardial function and mass are tightly linked to cardiac glucose metabolism we tested the hypothesis that expression and activation of the estrogen receptor α (ERα) might be required and sufficient to maintain physiological cardiac glucose uptake in the murine heart. Methods and Results: Cardiac glucose uptake quantified in vivo by 18F-fluorodeoxyglucose positron emission tomography (FDG-PET) was strongly impaired in ovarectomized compared to gonadal intact female C57BL/6JO mice. The selective ERα agonist 16α-LE2 and the non-selective ERα and ERβ agonist 17β-estradiol completely restored cardiac glucose uptake in ovarectomized mice. Cardiac FDG uptake was strongly decreased in female ERα knockout mice (ERKO) compared to wild type littermates. Biochemical assays, affymetrix cDNA array analysis, western blotting and immuno-staining of cardiac glucose transporters revealed a positive correlation of ERα dependent cardiac FDG uptake with preserved cardiac glucose transporter-1 expression and micro-vascular localization. Conclusions: Systemic activation of the ERα estrogen receptor is sufficient and its expression is required to maintain physiological glucose uptake in the murine heart, which is likely to contribute to known cardio-protective estrogen effects. total samples analysed are 20

2012-12-20 | E-GEOD-34807 | biostudies-arrayexpress

The estrogen receptor α is required and sufficient to maintain physiological glucose uptake in the mouse heart

2012-12-20 | GSE34807 | GEO

Identification of ChIP-seq and RIME grade antibodies for Estrogen Receptor alpha

Project description:Estrogen Receptor alpha (ERα) is a key driver of most breast cancers, and it is the target of endocrine therapies used in the clinic to treat women with ERα positive (ER+) breast cancer. The two methods ChIP-seq (chromatin immunoprecipitation coupled with deep sequencing) and RIME (Rapid Immunoprecipitation of Endogenous Proteins) have greatly improved our understanding of ERα function during breast cancer progression and in response to anti-estrogens. A critical component of both ChIP-seq and RIME protocols is the antibody that is used to pull down the bait protein. To date, most of the ChIP-seq and RIME experiments for the study of ERα have been performed using the sc-543 antibody from Santa Cruz Biotechnology. However, this antibody has been discontinued, thereby severely impacting the study of ERα in normal physiology as well as diseases such as breast cancer and ovarian cancer. Here, we compare the sc-543 antibody with other commercially available antibodies, and we show that 06-935 (EMD Millipore) and ab3575 (Abcam) antibodies can successfully replace the sc-543 antibody for ChIP-seq and RIME experiments.

2019-03-21 | PXD012930 | Pride

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [RNA-Seq]

Project description:Estrogen receptor-α (ERα) is an important driver of breast cancer and is the target for hormonal therapies, anti-estrogens and drugs that limit estrogen biosynthesis (aromatase inhibitors). Mutations in the ESR1 gene identified in metastatic breast cancer provide a potential mechanism for acquired resistance to hormone therapies. We have used CRISPR-Cas9 mediated genome editing in the MCF-7 breast cancer cell line, generating MCF-7-Y537S. MCF-7-Y537S cells encode a wild-type (tyrosine 537) and a mutant (serine 537) allele. Growth of the line is estrogen-independent and expression of ERα target genes is elevated in the absence of estrogen. ER ChIP-seq was carried out to map global ERα binding sites in the presence and absence of estrogen. RNA-seq following estrogen treatment was used for gene expression analysis. We show that expression of ER target genes and ER recruitment to ER binding regions is similar in MCF-7 and MCF-7-Y537S cells, except that ER recruitment to DNA and expression of ER target genes is frequently elevated in the absence of estrogen.

2016-10-25 | GSE78285 | GEO

Modeling the ESR1 tyrosine 537 mutation with CRISPR-Cas9 for mechanistic studies and evaluation of therapeutic approaches for metastatic breast cancer [ChIP-Seq]

2016-10-25 | GSE78284 | GEO

Transcriptional changes in response to 17β-estradiol, cigarette sidestream smoke particulates, and TNFα treatments in ERα-induced and uninduced CL1-5(TO-ERα) cells

Project description:This microarray analysis was designed to determine (1) the impact of ERα expression on cellular TNFα response and estrogen-TNFα signaling crosstalk and (2) whether cigarette sidestream smoke particulates had estrogen-like action in human lung adenocarcinoma cells. The lung adenocarcinoma cell line CL1-5(TO-ERα)#18 was used as a model. Expression of ERα in this cell line is under Tet-on regulation and can be induced by addition of doxycycline. For the Objective 1, we found three types of TNFα responsive genes: estrogen/ERα-dependent, estrogen/ERα-enhanced, and estrogen/ERα-independent. For the Objective 2, the microarray data revealed that cigarette sidestream smoke particulates regulated given genes via ERα as 17β-estradiol in lung adenocarcinoma cells. Some of these ERα target genes had been identified previously.

2020-10-07 | GSE67475 | GEO

Expression data for Control and SMRT-Depleted MCF-7 Cells

Project description:Estrogens are an important regulator of breast cancer disease progression, and they function by binding the estrogen receptor-α (ERα) to regulate changes in gene expression. ERα is able to both activate and inhibit gene transcription in a gene-specific manner and do so by binding target DNA sequences and recruiting coactivators and corepressors which can modulate the chromatin environment. Silencing mediator of retinoic acid and thyroid hormone receptor (SMRT) is known to act as coactivator and corepressor of ERα in a gene-specific manner. We used a microarray analysis to examine the gene expression changes that occur when the coregulator SMRT is depleted from the ERα positive MCF-7 breast cancer cell line.

2014-06-21 | GSE57935 | GEO

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