Transcriptome profiling of de-differentiated chondrocytes over-expressing miR-138 or miR-181ab1 during osteogenic induction
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ABSTRACT:
PROVIDER: PRJNA429652 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6464760.fastq.gz | Fastqsanger.gz | |||
| SRR6464770.fastq.gz | Fastqsanger.gz | |||
| SRR6464780.fastq.gz | Fastqsanger.gz | |||
| SRR6464790.fastq.gz | Fastqsanger.gz | |||
| SRR6464800.fastq.gz | Fastqsanger.gz |
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Project description:The goal of this study was to investigate the effects of miR-138 or miR-181ab1 on regulating osteogenesis. Gene expression profiles were analyzed in human de-differentiated chondrocytes (DDCs) over-expressing either miR-138 or miR-181ab1 following day 2 or day 7 of osteogenic induction. DDCs were isolated from human osteoarthritic articular cartilage and over-expression of miR-138 or miR-181ab1 was induced following lentiviral transduction of DDCs over-expressing the precursor form of miR-138 or miR-181ab1. Control DDCs were transduced with lentivirus expressing a non-silencing (NS) control RNA. Total RNA was harvested at day 2 or day 7 following osteogenic induction and subjected to RNA-Seq analysis.
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Project description:The goal of this study was to investigate the effects of miR-138 or miR-181a/b-1 on regulating chondrogenesis. Gene expression profiles were analyzed in human cartilage progenitor cells (CPCs) over-expressing either miR-138 or miR-181a/b-1 following 7 days of chondrogenic induction in high cell density pellet cultures under hypoxic conditions (5% O2). CPCs were isolated from human osteoarthritic articular cartilage and over-expression of miR-138 or miR-181a/b-1 was achieved via lentiviral transduction of the precursor form of miR-138 or miR-181a/b-1. Control CPCs were transduced with lentivirus expressing a non-silencing (NS) control RNA sequence. Total RNA was harvested at day 7 of chondrogenic induction and subjected to RNA-Seq analysis.
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Project description:We previously showed that miR-138 can repress herpes simplex virus 1 (HSV-1) ICP0 expression by binding to ICP0 mRNA. However, in this study we found that miR-138 can also repress viral gene expression independent of ICP0. We did not find other confirmed viral targets of miR-138. Therefore we conducted these RNAseq experiments (in combination with PAR-CLIP experiments whose results are uploaded separately) to identify host targets of miR-138 in two cell lines to explain the ICP0-independent effects on HSV-1 gene expression.
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Project description:Like herpes simplex virus 1 (HSV-1) ICP0 mRNA, HSV-2 ICP0 mRNA is predicted to be targeted by a host neuron-specific microRNA, miR-138. This study was designed to confirm the interaction between HSV-2 ICP0 mRNA and miR-138, and to identify other potential viral and host targets of miR-138 during HSV-2 infection. We performed PAR-CLIP on HSV-2 infected 293T cells overexpressing miR-138 in comparisin to control 293T cells. The results confirmed ICP0 as miR-138's targets, and also identified some other potential viral and host targets of miR-138.
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Project description:Analysis of mouse chondrocytes lacking the microRNA-140. MicroRNAs are genomically encoded small RNAs to regulate the gene expression. miR-140 shows high expression in cartilage. Results provide insight into the molecular mechanisms underlying miR-140 function in chondrocytes. Keywords: Expression profiling by array DNA microarray analysis was performed using Affymetrix mouse genome 430 2.0 array. RNA samples collected from cultured rib chondrocytes of wild-type and miR-140-/- to identify potential mRNA targets of miR-140. 2 M-BM-5g of total RNA was reverse transcribed with SuperScript II and second strand cDNA was synthesized. Biotinylated antisense cRNAs was amplified and transcribed using the GeneChip expression 3M-bM-^@M-^Y-Amplification reagent (Affymetrix). Finally, 10 M-BM-5g of cRNAs were fragmented and hybridized to GeneChip (R) Mouse Genome 430 2.0 array (Affymetrix). Microarray data were summarized by Robust Multichip Average (RMA) method and statistical analysis was performed using NIA Array Analysis (http://Igusun.grc.nia.nih.gov/ANOVA/).
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