Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA138521 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury.
2012-04-04 | GSE27642 | GEO
Project description:The molecular mechanisms of acute lung injury are incompletely understood. MicroRNAs (miRNAs) are crucial biological regulators that act by suppressing their target genes and are involved in a variety of pathophysiologic processes. MiR-127 appeared to be down-regulated during lung injury. We set out to investigate the role of miR-127 in lung injury and inflammation. Expression of miR-127 significantly reduced cytokine release by macrophages. Looking into the mechanisms of the regulation of inflammation by miR-127, we found that IgG Fcγ Receptor I (FcγRI/CD64) was a target of miR-127, as evidenced by reduced CD64 protein expression in macrophages over-expressing miR-127. Furthermore, miR-127 significantly reduced the luciferase activity with a reporter construct containing the native 3’-UTR of CD64. Importantly, we demonstrated that miR-127 attenuated lung inflammation in an IgG immune complex (IgG IC) model in vivo. Collectively, these data show that miR-127 targets macrophage CD64 expression and promotes the reduction of lung inflammation. Understanding how miRNAs regulate lung inflammation may represent an attractive way to control inflammation induced by infectious or non-infectious lung injury. MH.S-miR127 and MH.S-Sico cells were cultured for RNA extraction.Total RNA were assessed for quality with Agilent 2100 Bioanalyzer G2939A (Agilent Technologies,Santa Clara, CA)) and Nanodrop 8000 spectrophotometer (Thermo Scientific/Nanodrop, Wilmington, DE). Hybridization targets were prepared with MessageAmp™ Premier RNA Amplification Kit (Applied Biosystems/Ambion, Austin, TX) from total RNA, hybridized to GeneChip® Mouse Genome 430 2.0 arrays in Affymetrix GeneChip® hybridization oven 645, washed in Affymetrix GeneChip® Fluidics Station 450 and scanned with Affymetrix GeneChip® Scanner 7G according to standard Affymetrix GeneChip® Hybridization, Wash, and Stain protocols. (Affymetrix, Santa Clara,CA).
2012-04-03 | E-GEOD-27642 | biostudies-arrayexpress
Project description:Atopic asthma is a chronic inflammatory disease of the lungs that is commonly associated with a Th2 response. The role of allergen-specific IgG in the initiation and development of allergic airway inflammation is still poorly understood; however, a receptor of IgG-immune complexes, CD16, has been demonstrated to promote augmentation of Th2 responses. To identify what genes downstream of CD16 signaling may be contributing to development of a Th2 response, we use ovalbumin (OVA) as our model antigen and compared wildtype and CD16-/- BMDCs that were treated overnight with OVA or OVA-immune complex. C57Bl/6 and CD16-/- BMDCs were treated for 24 hours with OVA or OVA-immune complex and then analyzed for gene expression changes.
2013-02-20 | E-GEOD-44388 | biostudies-arrayexpress
Project description:Atopic asthma is a chronic inflammatory disease of the lungs that is commonly associated with a Th2 response. The role of allergen-specific IgG in the initiation and development of allergic airway inflammation is still poorly understood; however, a receptor of IgG-immune complexes, CD16, has been demonstrated to promote augmentation of Th2 responses. To identify what genes downstream of CD16 signaling may be contributing to development of a Th2 response, we use ovalbumin (OVA) as our model antigen and compared wildtype and CD16-/- BMDCs that were treated overnight with OVA or OVA-immune complex.
2013-02-20 | GSE44388 | GEO
Project description:We observed that proteasome regulator PSME4 inhibits antigen presentation and reduces cellular inflammation in lung adenocarcinoma. As tumor inflammation and antigenicity are key to anti-tumor immunity, we examined the effect of PSME4 in vivo by injecting mice with either KP1.9 or KP1.9PSME4_KD lung adenocarcinoma. We analyzed the changes in the immune milieu by performing single cell RNA sequencing (sc-RNA seq) of CD45+ cells, 3 weeks following injection of tumor cells. This allowed us to examine the effect of PSME4 on the early immune response to the tumor.
2023-03-04 | E-MTAB-10745 | biostudies-arrayexpress
Project description:MicroRNAs (miRNAs) are small non-coding RNAs that play a crucial role in post-transcriptional gene regulation. They are key regulators in various biological processes, including skeletal development and homeostasis. Disruptions in osteogenic differentiation pathways can lead to skeletal disorders such as osteoporosis and delayed fracture healing. MiR-127, initially identified for its tumor suppressor functions, has been already associated with skeletal disorders, but its direct role in regulating osteogenesis is still not fully understood. In this study, we demonstrated that overexpression of miR-127-3p using a miRNA mimics, significantly inhibits the in vitro osteogenesis of human bone marrow-derived mesenchymal stromal cells (hBMSCs). We observed reduced alkaline phosphatase activity and mineralization, along with decreased expression of bone marker genes. Additionally, pathway enrichment analysis from RNA sequencing at day 7 of osteogenesis indicated downregulation of cell cycle- and proliferation-related processes, which was confirmed by an BrdU incorporation assay. Also, upregulation of inflammation- and cell adhesion-related pathways was observed, and we were able to confirm the upregulation of Notch pathway by RT-qPCR. In conclusion, miR-127-5p inhibits the osteogenic differentiation and mineralization of hBMSCs.
2025-12-18 | GSE274022 | GEO
Project description:Demethylzeylasteral inhibits oxidative phosphorylation complex biogenesis by targeting LRPPRC in lung cancer
| PRJNA1170897 | ENA
Project description:Our previous study has showed that complex of NF90 and nuclear factor 45 (NF45) (NF90-NF45) inhibits miRNA biogenesis through negative regulation of primary-miRNA processing step. On the other hand, miRNAs, the biogenesis of which is regulated by NF90-NF45 in hepatocellular carcinoma, are not clear. Thus, to identify the miRNAs, we performed a miRNA array using RNAs extracted from control Huh7 cells and the cells depleted of NF90. Comparison of miRNA expression profile in one non-targeting control siRNA (siNTC)- or two independent siNF90-treated Huh7 cells.
2015-03-31 | E-GEOD-67411 | biostudies-arrayexpress
Project description:We recently showed that the mammalian genome encodes more than a thousand large intergenic non-coding RNAs (lincRNAs) that are clearly conserved across mammals and thus functional. Gene expression patterns have implicated these lincRNAs in diverse biological processes including cell cycle regulation, immune surveillance, and embryonic stem cell pluripotency. However, the mechanism by which these lincRNAs function is unknown. Here, we expand the catalog of human lincRNAs to ~3300 by analyzing chromatin-state maps of various human cell types. Inspired by the observation that the well-characterized lincRNA HOTAIR bind the Polycomb Repressive Complex 2 (PRC2), we tested whether many lincRNAs are physically associated with PRC2. Remarkably, we observe that ~20% of lincRNAs expressed in various cell types are bound by PRC2, and that additional lincRNAs are bound by other chromatin-modifying complexes. Moreover, we show that siRNA-mediated depletion of certain lincRNAs associated with PRC2 leads to changes in gene expression and that the upregulated genes are enriched for those normally silenced by PRC2. We propose a model in which some lincRNAs guide chromatin–modifying complexes to specific genomic loci to regulate gene expression. siRNA-mediated lincRNA knockdown siRNAs targeting specific lincRNAs were transected into human fibroblasts. Non-targeting siRNAs were used as controls. Both of these experiment types were hybridized to Affymetrix gene expression arrays. PRC2 RIP-Chip The PRC2 complex was immunoprecipitated using antibodies targetting Suz12 and the associated RNA was hybridized to Nimblegen tiling arrays representing lincRNAs. In parallel an IgG IP was performed and hybridized to the same NG arrays. RIP was performed for PRC2 and hybridized using a Cy3 label. In parallel, RIP was performed using IGG and labelled with Cy5 PRC2 RIP-Chip (dye swap) The PRC2 complex was immunoprecipitated using antibodies targetting Suz12 and the associated RNA was hybridized to Nimblegen tiling arrays representing lincRNAs. In parallel an IgG IP was performed and hybridized to the same NG arrays. RIP was performed for PRC2 and hybridized using a Cy5 label. In parallel, RIP was performed using IGG and labelled with Cy3 PRC2 RIP-Chip (no proteins) The PRC2 complex was immunoprecipitated using antibodies targetting Suz12 and the associated RNA was hybridized to Nimblegen tiling arrays representing lincRNAs. In parallel an IgG IP was performed and hybridized to the same NG arrays. RIP was performed for PRC2 and hybridized using a Cy3 label. In parallel, RIP was performed using IGG and labelled with Cy5 COREST RIP-Chip The COREST complex was immunoprecipitated using antibodies targetting COREST and the associated RNA was hybridized to Nimblegen tiling arrays representing lincRNAs. In parallel an IgG IP was performed and hybridized to the same NG arrays. RIP was performed for COREST and hybridized using a Cy3 label. In parallel, RIP was performed using IGG and labelled with Cy5 H3K27me3 and H3K4me2 modified histones RIP-Chip The H3K27me3 and H3K4me2 modified histones were immunoprecipitated using antibodies targetting COREST and the associated RNA was hybridized to Nimbelgen tiling arrays representing lincRNAs. In parallel an IgG IP was performed and hybridized to the same NG arrays. RIP was performed for COREST and hybridized using a Cy3 label. In parallel, RIP was performed using IGG and labelled with Cy5 Human lincRNA expression Human lincRNAs were profiled in HeLa, Lung FB, and Foot FB. In addition, nuclear and cytoplasmic fractions were taken in HeLa cells Total RNA was extracted from HeLa, Foot, and Lung cells and hybridized to NG tiling array. In addition, the nucleus was fractionated and RNA was hybridized to an array.
2009-07-09 | E-GEOD-16226 | biostudies-arrayexpress