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The miR-183/96/182 cluster is a checkpoint for resident immune cells and shapes the cellular landscape of the cornea.

ABSTRACT: The conserved miR-183/96/182 cluster (miR-183C) regulates both corneal sensory innervation and corneal resident immune cells (CRICs). This study is to uncover its role in CRICs and in shaping the corneal cellular landscape at a single-cell (sc) level.

ORGANISM(S): Mus musculus

PROVIDER: GSE249384 | GEO | 2024/01/10

REPOSITORIES: GEO

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The miR-183/96/182 Cluster Regulates Sensory Innervation, Resident Myeloid Cells and Functions of the Cornea Through Cell type-specific Target Genes

Project description:The miR-183/96/182 cluster (miR-183C) is specifically expressed in sensory neurons and immune cells and modulates corneal immune/inflammatory response to bacterial infection. To uncover the roles of miR-183C in corneal homeostasis through its regulation of sensory neurons of the trigeminal ganglia (TG) and innate myeloid cells, we created miR-183C conventional knockout (KO), and sensory nerve-specific (SNS-CKO) and myeloid cell-specific conditional knockout (MS-CKO) mice. We performed 3'RNA sequencing in the TG and corneas of these knockout mice and their wild type (WT)-control littermates. To study specific functions of miR-183C in corneal resident myeloid cells (CRMCs), we isolated Csf1r-EGFP+ CRMCs from conventional KO and MS-CKO and their WT control mice. By comparison of the gene expression profiles of the KO or CKO vs their corresponding WT mice, we identified a series of differentially expressed genes. Bioinformatic analyses uncovered tissue- and/or cell-type-specific target genes of miR-183C. Functional annotation of the target genes revealed functions of miR-183C in TG and CRMCs.

2023-12-20 | GSE250213 | GEO

The microRNA cluster miR-183/96/182 contributes to long-term memory in a protein phosphatase 1 dependent manner

Project description:Memory formation is a complex cognitive function regulated by coordinated synaptic and nuclear processes in neurons. In mammals, it is controlled by multiple molecular activators and suppressors, including the key signaling regulator protein phosphatase 1 (PP1). Here, we show that memory control by PP1 involves the miR-183/96/182 cluster, which is selectively regulated during memory formation. Inhibiting nuclear PP1 in mice brain or training in object recognition task similarly increases miR-183/96/182 expression in the hippocampus. Mimicking this increase by overexpressing miR-183/96/182 enhances object memory, while suppressing endogenous level of the cluster reduces it. This effect involves the modulation of many plasticity-related genes, and we identified HDAC9 as one of the functional targets. Further, PP1 controls miR-183/96/182 in a transcription-independent manner influencing processing of their precursors. These findings provide novel evidence for the role of miRNAs in memory formation and suggest the implication of PP1 in miRNAs processing in the adult brain.

2016-09-20 | GSE83707 | GEO

Regulation of Th17 cell pathogenic function by miR-183/96/182

Project description:Th17 cells are key players in autoimmune diseases. However, the roles of non-coding RNAs in Th17 cells are largely unknown. Here, we show that deletion of the Dicer gene specifically in Th17 cells protects from experimental autoimmune encephalomyelitis (EAE). Th17 cells highly express the miR-183/96/182 cluster (miR-183C), in response to IL-6/STAT3 signaling. Moreover, miR-183C regulates pathogenic cytokine expression during Th17 development. Furthermore, transcription factor Foxo1 is one of functional targets of miR-183C in Th17 cells: Foxo1 negatively regulates the pathogenicity of Th17 cells and miR-183C represses Foxo1 expression. Collectively, our results demonstrate one of crucial roles for miR-183C cluster in regulation of Th17 cell function in autoimmune diseases.

2016-06-21 | GSE78505 | GEO

A mouse model of miR-96, miR-182 and miR-183 misexpression implicates miRNAs in cochlear cell fate and homeostasis

Project description:Transgenic FVB/NCrl-Tg(GFAP-Mir183,Mir96,Mir182)MDW1 mice (Tg1MDW) overexpress this neurosensory-specific miRNA cluster in the inner ear and were developed as a model system to identify target genes and biologic processes regulated by the miR-183 cluster. Affymetrix mRNA microarray data analysis revealed that downregulated genes in P5 Tg1MDW/1MDW cochlea are statistically enriched for evolutionarily conserved predicted miR-96, miR-182 or miR-183 target sites.

2018-02-28 | GSE95579 | GEO

Modulation of the microRNA cluster miR-183-96-182 expression by the Epstein-Barr virus latent membrane protein 1

Project description:Epstein-Barr virus (EBV) is an oncogenic human herpesvirus involved in the pathogenesis of Burkitt’s lymphoma (BL) and various other lymphoproliferative disorders. In BL, EBV protein expression is restricted to the EBNA-1, but small non-coding RNAs such as the EBERs and micro (mi)RNAs can also be detected. miRNAs play major roles in crucial processes such as proliferation, differentiation and cell death. It has recently become clear that alteration in the expression profile of miRNAs contribute to the pathogenesis of a number of malignancies. During latent infection, EBV expresses 25 viral pre-miRNAs and modulates the expression of specific cellular miRNAs, such as miR-155 and miR-146, which potentially play a role in oncogenesis. Here, we established the small RNA expression profiles of three BL cell lines. Using large-scale sequencing coupled to northern blot and real-time RT-PCR analysis validation, we demonstrated the differential expression of some cellular and viral miRNAs. High-level expression of the miR-183-96-182 cluster and EBV miR-BART cluster was significantly associated with EBV type I latency. This expression was not affected by viral reactivation since TGF-ß1 stimulation did not significantly change the miRNA profiles. However, the expression of latent membrane protein (LMP)-1 triggered down-regulation of the expression of the miR-183-96-182 cluster. We further show that this effect involves the AKT signaling pathway.

2015-09-25 | GSE65752 | GEO

miR-182 and miR-183 act as GDNF mimics in midbrain neurons

Project description:We found in primary midbrain neurons the expression of miR-182 and miR-183 is increased with the treatment of GDNF. Further we showed that the transfaction with these two miRNA mimics resulted into the increased neurite length and regeneration in vitro. These mimics also showed neuroprotection of dopamenergic neurons in vitro and in vivo with an effect similar to GDNF. Finally we showed this effect is mediated by the downregulation of Foxo transcription factors.

2020-01-11 | GSE109066 | GEO

Gene expression profiling of miR-183/96 knock out mouse cochlea

Project description:Transcriptome analysis of P16 cochlea from wild type and miR-183/96 Knock out mice Gene expression analysis of miR-183/96 KO cochlea revealed a set of hair cell-relevant differentially expressed genes that could adversely impact hair cell physiology and contribute to the observed phenotype.

2018-05-01 | GSE106599 | GEO

miR-182 and miR-183 act as GDNF mimics in midbrain neurons

Project description:miR-182 and miR-183 act as GDNF mimics in midbrain neurons

| PRJNA429563 | ENA

Expression data from the RWPE-1 prostate epithelial cell line overexpressing the miR-183 family cluster

Project description:The full genomic miR-183 cluster (4.8kb) was cloned into lentiviral vector CD511B-1 with polycistronic GFP. RWPE-1 were transduced with a lentivirus from this vector (RWPE-1 183FC), or a CD511B-1 scrambled control with polycistronic GFP (RWPE-1 control). RWPE-1 were FACS sorted by GFP expression and expanded in culture. In RWPE-1 183FC, the miR-183 family members, miR-182, miR-96, and miR-183 were confirmed to be over-expressed at physioloically relevent levels, similar to the increased expression observed in prostate cancer epithelium.

2017-05-23 | GSE99134 | GEO

Inhibitory effect of miR-183 on MCM family members

Project description:MYCN and HDAC2 jointly repress the transcription of tumor suppressive micro RNA miR-183 in neuroblastoma. Enforced miR-183 expression induces neuroblastoma cell death and inhibits anchorage-independent colony formation and subcutaneous xenograft growth in mice. We here aimed to unravel the miR-183 signaling network and elucidated the role of MYCN mediated transcriptional activation of members of the minichromosome maintenance (MCM) family protein family involving miR-183 . The hexamer protein complex formed by MCM proteins is involved in the initiation and elongation of eukaryotic genome replication, thereby contributing to genomic integrity. Analysis of miR-183 versus negative control transfected neuroblastoma cells identified 85 differentially expressed proteins in a label-free mass spectrometric approach. Six members of the MCM family were found to be lower expressed upon enforced miR-183 expression, and subsequent annotation category enrichment analysis revealed a 14-fold enrichment in the protein module category “MCM”. Down-regulation was confirmed by western blot analysis. MicroRNA target prediction software studies revealed that miR-183 was predicted to directly target several MCMs.

2016-06-01 | PXD003596 | Pride

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