Analysis of the regulation of gene expression profiles by retinoblastoma-1 in Sertoli cells. Conditional knockout of Rb1 in Sertoli cells led to progressive infertiliy in male mice that occured between 10 and 14 weeks of age. Results of gene expression studies performed on 6 week-old purified Sertoli cells helped elucidate the key role of RB1 in mature, differentiated Sertoli cells.
Retinoblastoma protein plays multiple essential roles in the terminal differentiation of Sertoli cells.
Age, Specimen part
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Gene reactivation by 5-aza-2'-deoxycytidine-induced demethylation requires SRCAP-mediated H2A.Z insertion to establish nucleosome depleted regions.
Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesEpithelial-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.
Dysregulation of uterine signaling pathways in progesterone receptor-Cre knockout of dicer.
Age, Specimen part
View SamplesMaternal obesity during the pre-implantation period leads to a pro-inflammatory milieu in the ovaries. We conducted a global transcriptomic profiling in ovaries from TEN fed rats during the pre-implantation period. Microarray analysis revealed that obesity lead to increased expression of genes related to inflammation, decreased glucose transporters, and dysregulation of ovarian function-related genes in the ovaries. Our results suggest maternal obesity led to an up-regulation of inflammatory genes and Egr-1 protien expression in peri-implantation ovarian tissue, and a concurrent down-regulation of glucose transporters mRNA and AKT and PI3K protein levels.
Maternal obesity is associated with ovarian inflammation and upregulation of early growth response factor 1.
Sex, Specimen part
View SamplesTime-series analysis of response to ribosome 28s damage at gene expression level
Early Response to the Plant Toxin Stenodactylin in Acute Myeloid Leukemia Cells Involves Inflammatory and Apoptotic Signaling.
Cell line, Treatment
View SamplesCUGBP1 and MBNL1 are developmentally regulated RNA-binding proteins that are causally associated with myotonic dystrophy type 1. Using HITS-CLIP anlysis, we found CUGBP1 and MBNL1 preferentially bind to alternatively spliced introns and exons, as well as to the 3' UTRs.
CUGBP1 and MBNL1 preferentially bind to 3' UTRs and facilitate mRNA decay.
Specimen part, Cell line
View SamplesMaternal obesity during pregnancy leads to a pro-inflammatory milieu in the placenta. We conducted a global transcriptomic profiling in BeWo cells following palmitic acid (PA, 500 uM) and/or TNF-alpha (10 ng/ml) treatment for 24 h. Microarray analysis revealed that placental cytotrophoblasts increased expression of genes related to inflammation, stress response and immediate-early factors in response to plamitic acid, TNF-alpha or a combination of both. Our results suggest that fatty acids and inflammatory cytokines induce inflammation in placental cells via activation of JNK-Egr-1 signaling.
Early growth response protein-1 mediates lipotoxicity-associated placental inflammation: role in maternal obesity.
Specimen part, Cell line
View SamplesThe yeast PMR1 (ATP2C1) gene codes for the eukaryotic prototype of a high affinity P-type ATPase required for Ca2+/Mn2+ transport into the Golgi. Cells lacking PMR1 exhibit multiple genetic interactions with genes involved in DNA recombination and replication, a fact that is not yet understood. We find that deletion of PMR1 causes a delay in DNA replication initiation, progression and G2/M transition and induces the transcriptional up-regulation of genes involved in cell cycle regulation, including CLB5 and SWE1. Interestingly, pmr1 clb5 double mutants exhibit a dramatic delay in DNA replication and increased DNA breakage, while endoreplication and the formation of multi-nucleated, giant yeast is observed in pmr1 swe1 cells. Because these phenotypes can be attributed to impeded Mn2+-pump function, we provide a model in which Mn2+ interferes with Mg2+ in the nucleus, and vice versa, Mg2+ interferes with Mn2+ in the Golgi. Consequently, cell cycle progression is challenged by aberrant catalytic activities of enzymes involved in replication and protein glycosylation.
Impaired manganese metabolism causes mitotic misregulation.
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Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.
Sex, Age, Specimen part
View SamplesChronic dietary aspartame may impair rodent insulin tolerance and may affect behavior. Previous studies have shown the aspartame effects may be modulated by developmental NMDA receptor antagonism. Present study was designed to assess effects of aspartame and NMDAR antagonism on components of the HPA axis.
Effect of developmental NMDAR antagonism with CGP 39551 on aspartame-induced hypothalamic and adrenal gene expression.
Sex, Age, Specimen part
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