Ontology highlight
ABSTRACT:
PROVIDER: PRJNA493626 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7909620.fastq.gz | Fastqsanger.gz | |||
| SRR7909630.fastq.gz | Fastqsanger.gz | |||
| SRR7909621.fastq.gz | Fastqsanger.gz | |||
| SRR7909631.fastq.gz | Fastqsanger.gz | |||
| SRR7909622.fastq.gz | Fastqsanger.gz |
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Project description:This study annotates the NGS reads in a Sertoli cell sncRNA library. In addition to known sncRNAs, we also identified numerous novel sncRNAs expressed by Sertoli cells. Our data suggest that the Sertoli cell sncRNA transcriptome predominantly consists of miRNAs, piRNA-like RNAs, tRNAs and snoRNAs. This study reports the first comprehensive annotation of the Sertoli cell sncRNA transcriptome. Sertoli cells were purified from post-natal day 6 C57Bl/6 mice using the STAPUT unit gravity sedimentation apparatus. Small RNA was isolated from cells and a cDNA library was generated for 454 sequencing. Sequences from FastA files were initially mapped to known sequences and the genome and subsequently annotated upon novel small RNA categorization.
2012-09-08 | E-GEOD-40692 | biostudies-arrayexpress
Project description:The human placenta is the composite of multiple cell types, each which contributes uniquely to placental function. Small non-coding RNAs (sncRNAs) are regulators of gene expression and can be cell-specific. The sncRNA transcriptome of individual placental cell types has not yet been investigated due to difficulties in their procurement and isolation. Using a custom sequencing method, we explored the expression of seven sncRNA species (miRNA, piRNA, rRNA, scaRNA, snRNA, snoRNA, tRNA) from whole chorionic villi and four major sample-matched FACS-sorted cell type (cytotrophoblast, stromal, endothelial, Hofbauer) samples from 9 first trimester and 17 term placentas. After normalization for technical variables, samples clustered primarily by cell type lineage. No sncRNAs were uniquely expressed by cell type, however, mean expression differed by cell type for 115 sncRNAs. Known placentally-expressed sncRNAs showed differing expression by cell type and trimester. Expression of few sncRNAs varied by sex. Lastly, sample-matched sncRNA expression and DNA methylation correlation was not significant, although high correlation (>R2±0.6) was observed for some sncRNA-CpG pairs. This study represents the first exploration of the sncRNA transcriptome of bulk placental villi and placental cell types, informing about the expression and regulatory patterns underlying human placental development.
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Project description:Background: Aberrant expression of small non-coding RNAs (sncRNAs), in particular microRNAs (miRNAs) and PIWI-interacting RNAs (piRNAs) define several pathological processes. Asthma is characterized by airway hyper-reactivity, chronic inflammation and airway wall remodeling. Asthma-specific miRNA profiles were reported for bronchial epithelial cells, but no information on sncRNA expression in asthmatic bronchial smooth muscle (BSM) cells is available. Objective: To determine whether primary BSM sncRNA expression profile is altered in asthma and identify targets of differentially expressed sncRNAs. Methods: SmallRNA sequencing was used for sncRNA profiling in BSM cells (8 asthma, 6 non-asthma). sncRNA identification and differential expression analysis was performed with iMir, . experimentally validated miRNA targets were identified with Ingenuity Pathway Analysis and putative piRNA targets with miRanda. Results: Asthmatic BSM cells showed abnormal expression of 32 sncRNAs (26 miRNAs, 5 piRNAs, and 1 snoRNA). Target prediction for deregulated miRNAs and piRNAs revealed experimentally validated and predicted mRNA targets expressed in the BSM cells. 38 of these mRNAs represent major targets for deregulated miRNAs and may play important roles in the pathophysiology of asthma. Interestingly, 6 such miRNAs were previously associated with asthma and/or considered as novel therapeutic targets for treatment of this disease. Signaling pathway analysis revealed involvement of these sncRNAs in increased cell proliferation via PTEN and PI3K/Akt signaling pathways. Conclusions: BSM cells from asthma patients are characterized by aberrant sncRNA expression that recapitulates multiple pathological phenotypes of these cells. Implications: sncRNA expression profiling performed in this study further improve our understanding of the molecular mechanisms underlying asthma-associated processes in lungs.
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