Expression data from uterine tissue of Egr1 knockout mice.
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ABSTRACT:
PROVIDER: PRJNA1128698 | ENA |
REPOSITORIES: ENA
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Project description:Microarrays have been widely used to study estrogen responses, as estrogen-induced transcriptome changes significantly impact the uterus. This study investigates the gene expression profiling of Egr1 knockout (KO) mice treated with estrogen. Our goal is to identify transcriptomic features that differ between estrogen-treated Egr1 knockout uteri and wild-type (WT) uteri. We examined the gene expression patterns of 17 samples, consisting of Egr1 KO and WT uteri, at different time points: before estrogen treatment (0 h) and after treatment at 3 h, 6 h, and 24 h, using the MouseWG-6 V2 platform. Our findings indicate that Egr1 KO uteri exhibit dysregulation in reproductive and immune systems compared to WT uteri, and we observed altered insulin growth factor and PARylation activity related to uterine proliferation.
2025-06-09 | GSE270888 | GEO
Project description:Epithelial-stromal interactions in the uterus are required for normal uterine functions such as pregnancy, and multiple signaling pathways are essential for this process. Although Dicer and microRNAs (miRNA) have been implicated in several reproductive processes, the specific role of Dicer and miRNA in uterine development is not known. To address the roles of miRNA in the regulation of these key uterine pathways, we generated a conditional knockout (cKO) of Dicer in the postnatal uterine epithelium and stroma using progesterone receptor (PR)-Cre. These Dicer cKO are sterile with small uteri, which demonstrate significant defects including absence of glandular epithelium and enhanced stromal apoptosis, beginning at postnatal day 15 with expression of Cre and deletion of Dicer. Although these mice had normal serum steroid hormone levels, critical uterine signaling pathways, including progesterone-responsive genes, Indian hedgehog signaling, and the Wnt/Beta-catenin canonical pathway, were dysregulated at the mRNA level. Gene expression profiling data from pools of Dicer cKO and control uteri groups, at 15 days. two group comparison
2012-08-14 | E-GEOD-39181 | biostudies-arrayexpress
Project description:Epithelial-stromal interactions in the uterus are required for normal uterine functions such as pregnancy, and multiple signaling pathways are essential for this process. Although Dicer and microRNAs (miRNA) have been implicated in several reproductive processes, the specific role of Dicer and miRNA in uterine development is not known. To address the roles of miRNA in the regulation of these key uterine pathways, we generated a conditional knockout (cKO) of Dicer in the postnatal uterine epithelium and stroma using progesterone receptor (PR)-Cre. These Dicer cKO are sterile with small uteri, which demonstrate significant defects including absence of glandular epithelium and enhanced stromal apoptosis, beginning at postnatal day 15 with expression of Cre and deletion of Dicer. Although these mice had normal serum steroid hormone levels, critical uterine signaling pathways, including progesterone-responsive genes, Indian hedgehog signaling, and the Wnt/Beta-catenin canonical pathway, were dysregulated at the mRNA level.
2012-08-15 | GSE39181 | GEO
Project description:CDK7 adipose tissue specific knockout mice
| PRJNA627425 | ENA
Project description:Histone proteins undergo various modifications that alter chromatin structure, including addition of methyl groups. Enhancer of homolog 2 (EZH2), is a histone methyltransferase that methylates lysine residue 27, and thereby, suppresses gene expression. EZH2 plays integral role in the uterus and other reproductive organs. We have previously shown that conditional deletion of uterine EZH2 results in increased proliferation of luminal and glandular epithelial cells, and RNAseq analyses reveal several uterine transcriptomic changes in Ezh2 conditional (c) knockout (KO) mice that can affect estrogen signaling pathways. To pinpoint the origin of such gene expression changes, we used the recently developed spatial transcriptomics (ST) method with the hypotheses that Ezh2cKO mice would predominantly demonstrate changes in epithelial cells and/or ablation of this gene would disrupt normal epithelial/stromal gene expression patterns. Uteri were collected from ovariectomized adult WT and Ezh2cKO mice and analyzed by ST. Asb4, Cxcl14, Dio2, and Igfbp5 were increased, Sult1d1, Mt3, and Lcn2 were reduced in Ezh2cKO uterine epithelium vs. WT epithelium. For Ezh2cKO uterine stroma, differentially expressed key hub genes included Cald1, Fbln1, Myh11, Acta2, and Tagln. Conditional loss of uterine Ezh2 also appears to shift the balance of gene expression profiles in epithelial vs. stromal tissue toward uterine epithelial cell and gland development and proliferation, consistent with uterine gland hyperplasia in these mice. Current findings provide further insight into how EZH2 may selectively affect uterine epithelial and stromal compartments. Additionally, these transcriptome data might provide the mechanistic understanding and valuable biomarkers for human endometrial disorders with epigenetic underpinnings.
2021-08-17 | GSE181885 | GEO
Project description:The early growth response (Egr) family of transcriptional regulators consists of four closely related molecules (Egr1-4) that regulate target genes involved in cellular growth and differentiation. In the brain, Egr transcription factors have a critical role in learning and memory processing, presumably by regulating effector target genes that alter synaptic efficacy or mediate structural changes in neurons. Previous work suggests that Egr1 and Egr3 are the most important synaptic activity induced Egr molecules in the brain and they appear to have redundant regulatory function. How Egr transcriptional regulators influence learning and memory processing in the brain is unknown because target genes regulated by them have not been identified. Using Affymetrix microarray analysis and Egr loss-of-function mice, we will begin to characterize the gene regulatory networks modulated by Egr transcription factors in the brain. We anticipate that basic mechanisms related to transcriptional control of learning and memory related plasticity and the identification of plasticity effector molecules that may be involved in synaptic dysfunction associated with degenerative diseases or brain injury will result from these studies. To identify Egr transcription factor target gene regulation in brain: Target genes regulated by Egr transcription factors have not been identified in the brain, yet the transcription factors are essential for normal learning and memory processes. Using Egr1/3 double knockout and wild type littermate mice, we will compare gene expression profiles from somatosensory cortex to identify genes that are deregulated in Egr1/3 dKO brains. Egr1 and Egr3 gene expression is coupled to synaptic N-methyl D-aspartate (NMDA) receptor activation, mitogen activated protein kinase (MAPK) signaling engaged by NMDA receptor activation and long term synaptic potentiation (LTP). Previous studies have demonstrated defects in late phase LTP, long-term memory in hippocampal dependent tasks and reconsolidation of memories in Egr1-deficient mice, but the target effector molecules regulated by Egr transcription factors are not known. We hypothesize that it will be possible to identify Egr dependent target genes by using Affymetrix microarray analysis to compare gene expression from wild type cerebral cortex that has high levels of Egr protein expression with gene expression in cortex from Egr1/3 double knockout mice. Egr1 and Egr3 are highly expressed in mouse cortex and hippocampus twenty one days after birth because of the large amount of maternal stimulation they receive prior to weaning. We will compare the gene expression profile in somatosensory cortex from P21 wild type mice to that of P21 Egr1/3 dKO mice. We will perform microarray analysis using the Mouse 430 2.0 gene array with RNA samples from 3 wild type and 3 1/3 dKO brains (6 arrays total). Differentially regulated genes (up-regulated and down-regulated) will be identified from the list of genes with significantly altered expression greater than or equal to 2-fold by paired T test. Interesting genes will be validated by real-time PCR in wild type and 1/3 dKO brains. Our main goal is to identify genes that are directly regulated by Egr3. Recognizing that both direct and indirect target genes may be identified in the list of differentially expressed genes, real-time PCR validated target genes will be further screened using chromatin immunoprecipitation coupled with PCR (ChIP-PCR) to determine whether Egr1 and/or Egr3 are bound to potential regulatory regions of the putative target genes.
2008-06-13 | E-GEOD-4752 | biostudies-arrayexpress
Project description:Uterine transpriptome of pre-pubertal WT and ERa knockout (Ex3aERKO) mice
| PRJNA622804 | ENA
Project description:We sequenced strand-specific rRNA-depleted librairies performed from total RNAs isolated from subcutaneous inguinal fat pads of three 2-week-old wild-type female mice and three 2-week-old Egr1-deficient female mice.
2017-11-23 | GSE91058 | GEO
Project description:The functions of EGR1, a multifunctional transcription factor, in prostate cancer are well documented. However, little is known about the functions of EGR1 in lung cancer. we observed the function of EGR1 in non-small cell lung carcinoma (NSCLC) and identified the genes that influence cell fate and tumor development. We used microarrays to detail the global programme of gene expression and identified genes differentially expressed when EGR1-overexpressed. We have demonstrated that EGR1 is able to increase cell apoptosis, and inhibit metastasis. And we sought to find genes distributed to decrease the malignancy of human non-small cell lung cancer regulated by EGR1. To that end, H1299 cells were transfected either EGR1 or pcDNA3.1. After 48h, cells were collected for RNA extraction and hybridization on Affymetrix microarrays (PEGR1 VS PCDNA3.1).
2013-09-17 | E-GEOD-50913 | biostudies-arrayexpress
Project description:Human bone marrow stromal cells (BMSCs) are key elements of the hematopoietic environment and they play a central role in bone and bone marrow physiology. However, how key BMSC functions are regulated is largely unknown. We analyzed the role of the immediate early response transcription factor EGR1 as key BMSC regulator and found that EGR1 was highly expressed in prospectively-isolated primary BMSCs, downregulated upon culture, and lower in non-CFU-F-containing CD45neg BM cells. Furthermore, EGR1 expression was lower in proliferative regenerating adult and fetal primary cells compared to adult steady-state BMSCs. Accordingly, EGR1 overexpression markedly decreased BMSC proliferation but considerably improved hematopoietic stroma support function as indicated by an increased production of transplantable CD34+CD90+ hematopoietic stem cells in expansion co-cultures. The improvement of BMSC stroma support function was mediated by increased expression of hematopoietic supporting genes, such as VCAM1 and CCL28. On the other hand, EGR1 knockdown increased ROS-mediated BMSC proliferation, and clearly reduced BMSC hematopoietic stroma support potential. These findings thus show that EGR1 is a key BMSC transcription factor with a dual role in regulating proliferation and hematopoietic stroma support function that is controlling a genetic program to coordinate the specific functions of BMSC in their different biological contexts.
2019-06-27 | PXD011767 | Pride