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The effect of miR-204 on mRNA expression profiles of primary mouse chondrocytes

ABSTRACT: mRNA profiles of primary mouse chondrocytes transfected with miR-Ctrl or miR-204 mimics were generated by mRNA sequencing. This study provides insights into the role of miR-204 in chondrocytes.

ORGANISM(S): Mus musculus

PROVIDER: GSE126846 | GEO | 2019/02/22

REPOSITORIES: GEO

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RNA-seq analysis of mouse bone marrow-derived macrophages overexpressing miR-204-3p

Project description:Bone marrow-derived macrophages were transfected with miRNA-204-3p mimics or mimics negative control for 24 hours. RNA-seq was performed to compare miR-204-3p overexpression versus control cells.

2023-03-01 | GSE223129 | GEO

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MIR-204 target genes

Project description:The aim of this study is to discover genes regulated by miR-204. Differential gene expression in HEK-293 cells transfected with miR-204-mimic compared to HEK-293 cells transfected with control oligo (HEK-293 control) was analyzed using the Agilent Human Whole Genome 4x44K gene expression array (Agilent Technologies, Santa Clara, CA). HEK-293 cells were transfected with either miR-204 or a control, and gene expression was analyzed using the Agilent Human Whole Genome 4x44K array. A dye-swap was performed.

2012-03-30 | E-GEOD-28400 | biostudies-arrayexpress

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The effect of miR-204 on mRNA expression profiles of primary mouse chondrocytes

Project description:The effect of miR-204 on mRNA expression profiles of primary mouse chondrocytes

| PRJNA523504 | ENA

Genome-wide maps of chromatin state changes in miR-204-3p-overexpressed human monocyte-derived macrophages (HMDMs)

Project description:We compared histone modification states between miRNA-204-3p and mimics negative control transfected HMDMs through ChIP. sequencing

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Expression profile of HCT116 cells transfected with miR-204-5p

Project description:We have employed whole genome microarray expression profiling as a discovery platform to screen potential target genes of miR-204-5p in colorectal cancer cell HCT116. HCT116 cells were seeded in 6-cm2 tissue culture plates and transfected with the miR-204-5p mimic or negative control (NC) using Lipofectamine 2000 (Invitrogen, USA). After propagation for 48 hours, total RNA was extracted using TRIzol reagent (Invitrogen, USA). Expression profiling was performed using an Agilent human whole genome oligo microarray chip (4M-CM-^W44K) (Agilent, USA) Expression profiling in HCT116 cells was measured at 48 hours after transfection with miR-204-5p or negative control. Experiments were performed using the two samples without repeat experiment.

2014-07-30 | E-GEOD-59897 | biostudies-arrayexpress

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MiR-204-5p may Regulate Oxidative Stress in Myopia and Myopia-Related Retinopathy

Project description:Introduction: The mechanisms underlying myopia and myopia-related retinopathy remain not fully understood. We proposed to examine the function and underlying mechanisms of miR-204-5p in myopia development. Methods: The miR-204-5p expression level was assessed in the vitreous humor (VH) of a cohort consisting of 11 patients with high myopia (HM) and 16 control patients undergoing retinal surgery. The functional implications of miR-204-5p in ARPE-19 cells were assessed, encompassing cell aggressiveness. Thioredoxin-interacting protein (TXNIP) was found as a possible target of miR-204-5p through mRNA sequencing, and its interaction with miR-204-5p was confirmed employing luciferase assay and western blotting. Furthermore, the miR-204-5p function in regulating oxidative stress was examined by measuring reactive oxygen species (ROS) accumulation. Results: miR-204-5p was found to be significantly reduced in the VH of HM patients. Overexpression of miR-204-5p suppressed cell proliferation, migration, invasion, and apoptosis in ARPE-19 cells. The bioinformatics analysis demonstrated that miR-204-5p can modulate the genes associated with pathways relevant to myopia, including glycosaminoglycan (GAG) degradation, lysosome, and TGF−beta signaling pathway. The direct targeting of miR-204-5p on TXNIP has been confirmed through validation, and its downregulation mediated the miR-204-5p impacts on ARPE-19 cells. Moreover, miR-204-5p overexpression significantly reduced ROS accumulation by targeting TXNIP. Conclusion: Our findings revealed the possible contribution of the miR-204-5p/TXNIP axis in myopia development by regulating oxidative stress, which may provide new targets and novel therapeutic strategies to combat this prevalent and debilitating condition.

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