Mir-154 in mouse lung development
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA592989 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:mir-154 in mouse lung development - pull-down RNA
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Project description:mir-154 in mouse lung development - E18.5 in vivo data
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Project description:RNA isolated from MLE12 cells was subjected to a pull down assay with biotinilated miR-154 to enrich for miR-154 target mRNAs
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Project description:Transcription profiles from mice over expressing miR-154 (overExpr) were compared to profiles from mice with normal expression (control).
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Project description:miR154-3p and -5p are mainly expressed in the lung epithelium pre- and postnatally in mice and are significantly higher expressed upon hyperoxia (BPD mouse model). In normoxia in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to increased Fgf10 signaling and Tgf- signaling. Furthermore, avleolar morphometry revealed increased MLI indicating interference with alveologenesis at P16. In hyperoxia (P0-P8) in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to decreased Fgf10 signaling and Tgf- signaling.
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Project description:Identification of miR-154 downstream targets
| PRJNA593019 | ENA
Project description:We decompose the genome-wide expression patterns in 38 embryonic human lung (53-154 days post conception/dpc) into their independent, dominant directions of transcriptomic sample variation in order togain global insight of the developing human lung transcriptome.The characteristic genes and their corresponding bio–ontologic attribute profile for the latter were identified. We noted the over–representation of lung specific attributes (e.g., surfactant proteins) traditionally associated with later developmental stages, and highly ranked attributes (e.g., chemokine–immunologic processes) not previously reported nor immediately apparent in an early lung development context. We defined the 3,223–gene union of the characteristic genes of the 3 most dominant sources of variation as the developing lung characteristic sub–transcriptome (DLCS). It may be regarded as the minimal gene set describing the essential biology of this process. The developing lung series in this transcriptomic variation perspectiveform a contiguous trajectory with critical time points that both correlate with the 2 traditional morphologic stages overlapping -154 dpc and suggest the existence of 2 novel phases within the pseudoglandular stage. To demonstrate that this characterization is robust, we showed that the model could be used to estimate the gestational age of independent human lung tissue samples with a median absolute error of 5 days, based on the DLCS of their lung profile alone. Repeating this procedure on the homologous transcriptome profiles of developing mouse lung 14–19 dpc, we were able to recover their correct developmental chronology. Whole human fetal lung gene expression profiling from estimated gestational ages 53 to 154 days post conception. Keywords: Whole lung gene expression profiling, lung development, human fetus.
2009-09-10 | GSE14334 | GEO
Project description:The regulation of gene expression in cells, including by microRNAs (miRNAs), is a dynamic process. Current methods for identifying microRNA targets by combining sequence, miRNA and mRNA expression data do not adequately utilize the temporal information and thus miss important miRNAs and their targets. We developed a new method, mirDREM, that uses probabilistic modeling to reconstruct dynamic regulatory networks which explain how temporal gene expression is jointly regulated by microRNAs and transcription factors (TFs). We used mirDREM to study the regulation of postnatal lung development in mice. The reconstructed network for this process identified several known miRNAs and TFs and provided novel predictions about additional miRNAs and the specific developmental phases they regulate. Microarray data of Mouse Lung Epithelial cells MLE-12 after transfection with inhibitors for miR-30a, miR-30d, miR-23b and miR-125 and with precursors for miR-337, miR-466a, miR466d and miR-476c. The results provide a general insight into the gene expression profile which was modulated by the inhibition or overexpression of these microRNAs. We experimentally validated several predictions and show that miR-30d, miR-30a, and miR-467c are new regulators of proliferation in lung cells. Our analysis establishes new links between identified miRNAs and lung diseases, supporting recent evidence that such diseases may represent reversal of lung differentiation.
2013-10-18 | GSE41607 | GEO
Project description:The regulation of gene expression in cells, including by microRNAs (miRNAs), is a dynamic process. Current methods for identifying microRNA targets by combining sequence, miRNA and mRNA expression data do not adequately utilize the temporal information and thus miss important miRNAs and their targets. We developed a new method, mirDREM, that uses probabilistic modeling to reconstruct dynamic regulatory networks which explain how temporal gene expression is jointly regulated by microRNAs and transcription factors (TFs). We used mirDREM to study the regulation of postnatal lung development in mice. The reconstructed network for this process identified several known miRNAs and TFs and provided novel predictions about additional miRNAs and the specific developmental phases they regulate. Microarray data of Mouse Lung Epithelial cells MLE-12 after transfection with inhibitors for miR-30a, miR-30d, miR-23b and miR-125 and with precursors for miR-337, miR-466a, miR466d and miR-476c. The results provide a general insight into the gene expression profile which was modulated by the inhibition or overexpression of these microRNAs. We experimentally validated several predictions and show that miR-30d, miR-30a, and miR-467c are new regulators of proliferation in lung cells. Our analysis establishes new links between identified miRNAs and lung diseases, supporting recent evidence that such diseases may represent reversal of lung differentiation. We first analyzed the endogenous expression of miR-30a, miR-30d, miR-23b, miR-125, miR-337, miR-466a, miR466d and miR-476c in MLE-12 cells. Then, we transfected the MLE-12 cells with inhibitors ( miR-30a, miR-30d, miR-23b and miR-125) for the highly expressed and precursos for those that were almost undetectable (miR-337, miR-466a, miR466d and miR-476c). RNA level of the 8 microRNAs was verify by qRT-PCR in order to validate the transfection efficiency. Finally, 0.5ug of total RNA was used to performe the gene expression microarrays for each condition
2013-10-18 | E-GEOD-41607 | biostudies-arrayexpress
Project description:Using the highly sensitive miRNA array, we determined the serum miRNAs profiles of 10 non-smokers, 10 smokers and 10 lung cancer patients by miRCURY LNA™ microRNA Arrays. Differential expressed miRNAs were further validated in a larger scale samples. We found that let-7i-3p and miR-154-5p were significantly downregulation in serum of smokers and lung cancer patients. The serum level of let-7i-3p and miR-154-5p is associated with smoking and smoking-related lung cancer.
2014-06-17 | GSE58540 | GEO