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Homo sapiens

ABSTRACT: Analysis of Human Airway epithelial cells transcriptome after transfection of small RNAs from miR-34/449 family

PROVIDER: PRJNA309856 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR3126080.fastq.gz	Fastqsanger.gz
	SRR3126081.fastq.gz	Fastqsanger.gz
	SRR3126082.fastq.gz	Fastqsanger.gz
	SRR3126083.fastq.gz	Fastqsanger.gz
	SRR3126084.fastq.gz	Fastqsanger.gz

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Gene expression changes in the respiratory epithelium of miR-34/449 knockout mice

Project description:MicroRNA ablation prevents multiciliogenesis via cell cycle deregulation MicroRNAs (miRNAs) have been implicated in various biological processes but have been most frequently described to inhibit proliferation and tumorigenesis. Here we describe an essential function of the miR-34/449 family during differentiation of multiciliated cells that is mediated by their well-described suppression of cell cycle progression. Constitutive deletion of all six members of this miRNA family triggers a derepression of multiple cell cycle-promoting proteins, thereby preventing epithelial cells from exiting the cell cycle and to maintain in a quiescent state. As a result, formation of motile multicilia is strongly inhibited in several tissues including the respiratory epithelium and the fallopian tube. Consequently, mice lacking miR-34/449 genes display infertility as well as severe chronic airway disease leading to postnatal death. These results show how miRNA-mediated repression of the cell cycle is required to allow multiciliogenesis to proceed during epithelial differentiation.

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microRNAs-449 control vertebrate multi-ciliogenesis by repressing Notch signalling

Project description:This SuperSeries is composed of the following subset Series: GSE22141: MicroRNA signature during the time course of regeneration of the human airway mucociliary epithelium GSE22142: Transcriptome analysis during the time course of regeneration of the human airway mucociliary epithelium GSE22143: Transcriptomic impact of microRNAs-449 or microRNAs-34 overexpression in proliferating human airway epithelial cells GSE22144: miRNAs high throughput sequencing profiling of regenerating human airway epithelial cells GSE22145: miRNAs high throughput sequencing profiling of basals cells and columnar cells GSE22146: microRNAs signatures of Xenopus laevis embryo epidermis at stage 11 (non ciliated) and 26 (ciliated) using high throughput sequencing Refer to individual Series

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Project description:In this study, we comparatively analyzed the members of the miR-449 family (miR-449a, miR-449b, and miR-449c) with regards to their target genes and functional effects in hepatocellular carcinoma (HCC). Microarray analysis after transient transfection of miR-449a, miR-449b, and/or miR-449c in the HCC cell line HLE identified putative target genes of miR-449a, miR-449b, and miR-449c.

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Project description:Chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) are clinically and molecularly heterogeneous diseases. We utilized clustering and integrative network analyses to elucidate roles for microRNAs (miRNAs) and miRNA isoforms (isomiRs) in COPD and ILD pathogenesis. Short RNA sequencing was performed on 351 lung tissue samples of COPD (n=145), ILD (n=144) and controls (n=64). Five distinct subclusters of samples were identified including 1 COPD-predominant cluster and 2 ILD-predominant clusters which associated with different clinical measurements of disease severity. Utilizing 262 samples with gene expression and SNP microarrays, we built disease-specific genetic and expression networks to predict key miRNA regulators of gene expression. Members of miR-449/34 family, known to promote airway differentiation by repressing the Notch pathway, were among the top connected miRNAs in both COPD and ILD networks. Genes associated with miR-449/34 members in the disease networks were enriched among genes that increase in expression with airway differentiation at an air-liquid interface. A highly expressed isomiR containing a novel seed sequence was identified at the miR-34c-5p locus. 47% of the anticorrelated predicted targets for this isomiR were distinct from the canonical seed sequence for miR-34c-5p. Overexpression of the canonical miR-34c-5p and the miR-34c-5p isomiR with an alternative seed sequence down-regulated NOTCH1 and NOTCH4. However, only overexpression of the isomiR down-regulated genes involved in Ras signaling such as CRKL and GRB2. Overall, these findings elucidate molecular heterogeneity inherent across COPD and ILD patients and further suggest roles for miR-34c in regulating disease-associated gene-expression.

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Homo sapiens

Project description:Transcriptomic impact of microRNAs-449 or microRNAs-34 overexpression in proliferating human airway epithelial cells

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Project description:Transient transfection of miR-449 family in the hepatocellular carcinoma cell line HLE

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