To identify the relevant targets of the selected miRNAs, we assessed global transcriptome changes by deep-sequencing total neonatal mouse cardiomyocyte RNA after transfection with hsa-miR-590-3p or hsa-miR-199a-3p Overall design: Four condition experiment; one replicate per condition; mouse neonatal cardiomyocytes transfected with cel-miR-67, hsa-miR-590-3p and hsa-miR-199a-3p; samples collected 72 hours after transfection
Functional screening identifies miRNAs inducing cardiac regeneration.
Specimen part, Cell line, Treatment, Subject
View SamplesHeart failure is a leading cause of mortality and morbidity in the developed world, partly because mammals lack the ability to regenerate heart tissue. Whether this is due to evolutionary loss of regenerative mechanisms present in other organisms or to an inability to activate such mechanisms is currently unclear. Here, we decipher mechanisms underlying heart regeneration in adult zebrafish and show that the molecular regulators of this response are conserved in mammals. We identified miR-99/100 and Let-7a/c, and their protein targets smarca5 and fntb, as critical regulators of cardiomyocyte dedifferentiation and heart regeneration in zebrafish. Although human and murine adult cardiomyocytes fail to elicit an endogenous regenerative response following myocardial infarction, we show that in vivo manipulation of this molecular machinery in mice results in cardiomyocyte dedifferentiation and improved heart functionality after injury. These data provide a proof-of-concept for identifying and activating conserved molecular programs to regenerate the damaged heart. Overall design: RNA-Seq expression profiles of rat cardiomyocytes after knockdown of miR-99/100 and Let-7 miRNAs
In vivo activation of a conserved microRNA program induces mammalian heart regeneration.
No sample metadata fields
View SamplesTo determine effects of p53 activation on levels of RNA associated with polysomes, we performed RNA-seq analysis of colorectal carcinoma cell line HCT116, breast carcinoma line MCF7, and osteosarcoma line SJSA treated with MDM2 inhibitor Nutlin. Overall design: Polysomal RNA was extracted from HCT116, MCF7 and SJSA cells treated with Nutlin, polyA enriched and subjected to RNA-seq protocol.
Identification of a core TP53 transcriptional program with highly distributed tumor suppressive activity.
Cell line, Treatment, Subject
View SamplesIn order to understand the consequences of miR-210 blocking on the ischemia response, the transcriptomic changes were investigated by microarray technology in gastrocnemius muscles of ANTI-210 and SCR treated mice, 7 days after ischemia.
Hypoxia-Induced miR-210 Is Necessary for Vascular Regeneration upon Acute Limb Ischemia.
No sample metadata fields
View SamplesCase report of a twin pair with concordant JMML, but with a different disease course predicted by gene expression profiling
Different outcomes of allogeneic hematopoietic stem cell transplant in a pair of twins affected by juvenile myelomonocytic leukemia.
Specimen part, Disease
View SamplesHCT116 colon carcinoma cells invade more the basement membrane when carcinoma-associated fibroblasts (CAFs) are present. In order to identify if CAFs induce an invasive phenotype to HCT116 cells, and therefore regulate genes expression related to invasion, we compared gene expression of HCT116 cells cultured alone or in the presence of CAFs.
Cancer-associated fibroblasts induce metalloprotease-independent cancer cell invasion of the basement membrane.
Disease, Cell line
View SamplesTCP transcription factors from the CYC2-class are involved in the development of monosymmetric flowers in all core eudicot species analysed so far. In Antirrhinum majus, the CYC2/TCP transcription factor CYCLOIDEA (CYC) is the molecular key regulator driving the development of flower monosymmetry (Luo D, Carpenter R, Vincent C, Copsey L, Coen E: Origin of floral asymmetry in Antirrhinum. Nature 1996, 383:794-799). In the Brassicaceae Iberis amara, a stronger expression of the CYC2 gene IaTCP1 in the small adaxial petals likely leads to the reduced petal size in comparison to large abaxial petals, with hardly any IaTCP1 expression. This results in the formation of the monosymmetric Iberis flower (Busch A, Zachgo S: Control of corolla monosymmetry in the Brassicaceae Iberis amara. PNAS 2007, 104:16714-16719). In contrast, the orthologous TCP/CYC2 transcription factor TCP1 from Arabidopsis thaliana, which forms equally sized and shaped petal pairs, only shows an early and transient expression in the adaxial area of floral primordia. This implies that monosymmetry in the Brassicaceae evolved through a heterochronic expression shift of the TCP/CYC2 key regulator gene IaTCP1.
Differential transcriptome analysis reveals insight into monosymmetric corolla development of the crucifer Iberis amara.
Specimen part
View SamplesOver activation of the aryl hydrocarbon receptor (AhR) by TCDD results ampng other phenotypes in severe thymic atrophy accompanied by immunosuppression. The link between thymic atrophy, skewed thymocyte differntiation and immunosuppression is still not fully resolved. This study investigates the TCDD elicted exprssion changes in the ET, cortical thymus epithelial cell line.
Promoter analysis of TCDD-inducible genes in a thymic epithelial cell line indicates the potential for cell-specific transcription factor crosstalk in the AhR response.
Treatment, Time
View SamplesDose-dependent femoral gene expression was examined following repeated exposure (every 4 days for 28 days) to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). These data were used to examine the effect of repeated TCDD exposure on gene expression in the femur of C57BL/6 male mice. Overall design: Three biological replicates for each dose (0.01, 0.03, 0.1, 0.3, 1, 3, 10, 30) of TCDD and sesame oil vehicle
2,3,7,8-Tetrachlorodibenzo-p-dioxin dose-dependently increases bone mass and decreases marrow adiposity in juvenile mice.
Sex, Specimen part, Cell line, Treatment, Subject
View SamplesMicroarray data from G2-synchronized p53(+) and p53(-) fibroblasts before and after 3 h release from cell cycle blockade in the presence of 5 M sodium arsenite.
Exit from arsenite-induced mitotic arrest is p53 dependent.
No sample metadata fields
View Samples