Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.
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ABSTRACT:
PROVIDER: PRJNA718874 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14119965_1.fastq.gz | Fastqsanger.gz | |||
| SRR14119965_2.fastq.gz | Fastqsanger.gz | |||
| SRR14119966_1.fastq.gz | Fastqsanger.gz | |||
| SRR14119966_2.fastq.gz | Fastqsanger.gz | |||
| SRR14119967_1.fastq.gz | Fastqsanger.gz |
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Project description:Macrophage miR-210 induction and metabolic reprogramming in response to pathogen interaction boost life-threatening inflammation.
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2019-02-19 | E-MTAB-7697 | biostudies-arrayexpress
Project description:Similar with others, our data proved that antigen-specific CD8+ T cells from mice primed with DNA and boosted by VACV were much more sensitive to antigen stimulation than those from DNA-boost. Since the mechanisms of in vivo tuning of antigen sensitivity (also termed functional avidity) is still not defined, we compared this two vaccination regimen at gene expression level. Results provide important information of which genes were selectively activated by VACV boost vaccination. For example, data shows that the expression levels of genes involved in Cancer and Wnt signaling pathways is more higher in DNA prime-VACV boost regimen that DNA prime-DNA boost vaccination. To obtain sufficient of antigen-specific cells for microarray analysis, the OVA-specific CD8+ T cells from OT-1 mice were adoptively transferred into wild type mice and then immunized by DNA and VACV vaccine encoding OVA. Four week later, mice were scarificed and antigen-specific CD8+ T cells were emriched by CD45.1-PE antibody and anti-PE MicroBeads from splenocytes.Total RNA was extracted by the RNeasy Mini Kit (QIAGEN, Germany). Followed by amplification and biotin labeling, the samples were hybridized using Illumina Total Prep RNA Amplification Kit (Ambion, USA). Mouse WG-6v2 Expression BeadChips were used for analysis of transcriptome.
2013-10-30 | E-GEOD-51849 | biostudies-arrayexpress
Project description:mRNA profiling of miR-210 transgenic (in vivo), mimic-transfected (in vitro) and miR-210 knockout activated mouse B-cells was performed to assess the effect of miR-210 overexpression on the B-cell transcriptome.
2013-08-23 | E-MTAB-1758 | biostudies-arrayexpress
Project description:MicroRNAs are small non-coding RNA species, some of which are playing important roles in malignancies. However, roles of miR-210 in cancer have yet to be unknown and controversial. Here, we found the expression level of miR-210 is downregulated in human esophageal squamous cell carcinoma and its cell lines. Additionally, we demonstrate that miR-210 inhibits cancer cell survival and proliferation through upregulation of cell death and induction of cell cycle arrest at G1/G0 and G2/M phases. However, candidate target mRNAs of miR-210 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms.
2011-01-05 | GSE20637 | GEO
Project description:MicroRNAs are small non-coding RNA species, some of which are playing important roles in malignancies. However, roles of miR-210 in cancer have yet to be unknown and controversial. Here, we found the expression level of miR-210 is downregulated in human esophageal squamous cell carcinoma and its cell lines. Additionally, we demonstrate that miR-210 inhibits cancer cell survival and proliferation through upregulation of cell death and induction of cell cycle arrest at G1/G0 and G2/M phases. However, candidate target mRNAs of miR-210 and the mechanism behind observed phenomena is uncertain. Then, we performed comprehensive gene expression analysis to identify candidate target mRNAs and understand their mechanisms. KYSE-170 cells were transfected with oligoribonucleotides for miR-210 or ncRNA (Ambion, Austin, TX) using Hiperfect (Qiagen, Valencia, CA) according to the provider’s protocol for overexpression. Total RNA was extracted by the acid guanidinium thiocyanate-phenol-chloroform method and was labeled and prepared for hybridization to human Oligo chip 25k (Toray, Kamakura, Japan) using standard methods.
2011-01-05 | E-GEOD-20637 | biostudies-arrayexpress
Project description:Compulsory expression of miR-210 in normal endometrial stromal cells directed the induction of cell proliferation and vascular endothelial growth factor production, and the inhibition of apoptosis in through signal transducer and activator of transcription 3 (STAT3) activation. Accumulating evidence suggests that microRNAs play definite roles in the pathogenesis of endometriosis. The objective of the study was to determine the role of miR-210, one of the upregulated microRNA in endometriotic cyst stromal cells, in the pathogenesis of endometriosis. Downstream targets of miR-210 were identified by Compulsory expression of miR-210 in normal eutopic endometrial stromal cells, a global mRNA microarray technique, and Ingenuity pathways analysis.
2015-04-06 | GSE56854 | GEO
Project description:MicroRNAs (miRNAs) are small non-protein-coding RNAs that are incorporated into the RNA-induced silencing complex (RISC) and inhibit gene expression by regulating the stability and/or the translational efficiency of target mRNAs. Previously, we demonstrated that miR-210 is a key player of endothelial cell (EC) response to hypoxia, modulating EC survival, migration and ability to form capillary like-structures. Moreover, the receptor tyrosine kinase ligand Ephrin-A3 was identified as one functionally relevant target. Since each miRNA regulates hundreds of mRNAs, different approaches were combined to identify new miR-210 targets: a Using target prediction software, 32 new miR-210 potential targets were identified. b The proteomic profiling of miR-210 over-expressing ECs identified 11 proteins that were specifically inhibited by miR-210, either directly or indirectly. c Affymetrix based gene expression profiles identified 51 genes that were both down-modulated by miR-210 over-expression and de-repressed when miR-210 was blocked. Surprisingly, only few genes identified either by proteomics or transcriptomics were recognized as miR-210 targets by target prediction algorithms. However, a low-stringency pairing research revealed enrichment for miR-210 putative binding sites, raising the possibility that these genes were targeted via non-canonical recognition sequences. To clarify this issue, miR-210-loaded RISC was purified by immuno-precipitation along with its mRNA targets. The presence of Ephrin-A3 mRNA in the complex validated this approach. We found that 32 potential targets were indeed enriched in miR-210-loaded RISC, and thus can be considered as genuine miR-210 targets. In keeping with this conclusion, we were able to further validate a sub-set of them by 3’UTR-reporter assays. Gene ontology analysis of the targets confirmed the known miR-210 activity in differentiation and cell cycle regulation, highlighting new functions such as involvement in RNA processing, DNA binding, development, membrane trafficking and amino acid catabolism. In conclusion, we validated a multidisciplinary approach for miRNAs target identification and indicated novel molecular mechanisms underpinning miR-210 role in EC response to hypoxia.
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