In rodents, the uterus of a mature
Fine temporal analysis of DHT transcriptional modulation of the ATM/Gadd45g signaling pathways in the mouse uterus.
No sample metadata fields
View Samples17-Estradiol (E2) is well known to be associated with uterine cancer, endometriosis, and leiomyomas. Although insulin-like growth factor I (IGF-I) has been identified as a mediator of the uterotrophic effect of E2 in several studies, this mechanism is still not well understood. In the present study, identification of the genes modulated by a physiological dose of E2, in the uterus, has been done in ovariectomized mice using Affymetrix microarrays. The E2-induced genomic profile shows that multiple genes belonging to the IGF-I pathway are affected after exposure to E2. Two phases of regulation could be identified. First, from 0 to 6 h, the expression of genes involved in the cell cycle, growth factors, protein tyrosine phosphatases, and MAPK phosphatases is quickly upregulated by E2, while IGF-I receptor and several genes of the MAPK and phosphatidylinositol 3-kinase pathways are downregulated. Later, i.e., from 6 to 24 h, transporters and peptidases/proteases are stimulated, whereas defense-related genes are differentially regulated by E2. Finally, cytoarchitectural genes are modulated later. The present data show that a physiological dose of E2 induces, within 24 h, a series of transcriptional events that promote the uterotrophic effect. Among these, the E2-mediated activation of the IGF-I pathway seems to play a pivotal role in the uterotrophic effect. Furthermore, the protein tyrosine phosphatases and MAPK phosphatases are likely to modulate the estrogenic uterotrophic action by targeting, at different steps, the IGF-I pathway.
Temporal analysis of E2 transcriptional induction of PTP and MKP and downregulation of IGF-I pathway key components in the mouse uterus.
No sample metadata fields
View SamplesHematopoietic progenitor and stem cells from bone marrow have been sorted by FACS (LSK, Lineage -, Sca1 + and cKit +) and co-culture during 18h without cytokines with or without extracellular vesicles (EV) secreted by AFT stromal cells.
Extracellular vesicles of stromal origin target and support hematopoietic stem and progenitor cells.
Specimen part
View SamplesAn investigation of gene expression changes in rectal biopsies from donors with IBS compared to controls to begin to understand this complex syndrome. To further investigate differences between IBS groups (constipation and diarrhoea predominant) (part1) and how IBS relates to bacterial infection (part2) with biopsies taken 6 months after Campylobacter jejuni infection.
Identifying and testing candidate genetic polymorphisms in the irritable bowel syndrome (IBS): association with TNFSF15 and TNFα.
Sex, Specimen part, Disease, Subject
View SamplesAbnormal mitochondria metabolism and innate immune responses participate in the pathogenesis of many inflammatory disorders. The molecular events regulating mitochondrial activity to control survival and cell death in monocytes/macrophages are poorly understood. Here we show that miR-125b attenuates the activity of the mitochondrial respiratory chain through BIK silencing, and promotes the elongation of mitochondrial network through MTP18 targeting, without impacting autophagy, in the human monocytes. Proinflammatory activation is associated with a concomitant increase in miR-125b expression, decrease in BIK and MTP-18 expression, reduced oxidative phosphorylation, and enhanced mitochondrial fusion. Furthermore, expression of M1-associated transcripts as well as mitochondrial dynamics and energy metabolism are induced upon ectopic expression of miR-125b. In turn, by repressing miR-125b, mitochondrial dynamics was preserved, LPS-induced repression of BIK expression and of mitochondrial respiration were prevented, and M1 polarization of macrophages was inhibited. Altogether, our data reveal a novel role for miR-125b in controlling mitochondrial metabolism and dynamics by targeting BIK and MTP18, respectively, two novel cellular target proteins involved in maintaining the mitochondrial integrity in human monocytes. These findings not only suggest a novel function for miR-125b in regulating metabolic adaptation of monocytes to inflammation but also unravel new molecular mechanisms for its pro-apoptotic role and identify potential targets for interfering with inflammatory activation of monocytes.
miR-125b controls monocyte adaptation to inflammation through mitochondrial metabolism and dynamics.
Specimen part, Cell line
View SamplesPaneth cells recide in the intestinal crypt bottom and are part of the innate immunity and of the intestinal stem cell niche.
mTORC1 in the Paneth cell niche couples intestinal stem-cell function to calorie intake.
Age, Specimen part
View SamplesWe compared transcriptomes of two ependymoglial populations isolated from adult zebrafish telencephalon. Overall design: Ependymoglial cells are acutely isolated from the adult zebrafish brains form 3 months old transgenic gfap:GFP animals. GFP is experssed in all ependymoglial cells and two populations are separated using GFP intensity in FACS.
The Aryl Hydrocarbon Receptor Pathway Defines the Time Frame for Restorative Neurogenesis.
Specimen part, Subject
View SamplesSmall RNAs (sRNA) that act by base pairing with trans-encoded mRNAs modulate metabolism in response to a variety of environmental stimuli. Here, we describe an Hfq-binding sRNA (FnrS) whose expression is induced upon a shift from aerobic to anaerobic conditions and which acts to down regulate the levels of a variety of mRNAs encoding metabolic enzymes. Anaerobic induction in minimal medium depends strongly on FNR but is also affected by ArcA and CRP. Whole genome expression analysis showed that the levels of at least 32 mRNAs are down regulated upon FnrS overexpression, 15 of which are predicted to base pair with FnrS by TargetRNA. The sRNA is highly conserved across its entire length in numerous enterobacteria, and mutation analysis revealed that two separate regions of FnrS base pair with different sets of target mRNAs. The majority of the target genes previously reported to be down regulated in an FNR-dependent manner lack recognizable FNR binding sites. We thus suggest that FnrS extends the FNR regulon and increases the efficiency of anaerobic metabolism by repressing the synthesis of enzymes that are not needed under these conditions.
Reprogramming of anaerobic metabolism by the FnrS small RNA.
No sample metadata fields
View SamplesGene expression profiling in soybean under aluminum stress: genes differentially expressed between Al-tolerant and Al-sensitive genotypes.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
View SamplesGene expression profiling in soybean under aluminum stress: mechanisms of magnesium amelioration of aluminum toxicity at gene expression level.
Mechanisms of magnesium amelioration of aluminum toxicity in soybean at the gene expression level.
Specimen part, Treatment
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