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MiR-138 controls interneuron function and short-term memory

ABSTRACT: Using a miR-138 loss-of-function mouse model, a role for the brain enriched microRNA miR-138 in the regulation of inhibitory synaptic transmission and short-term memory formation was shown.

ORGANISM(S): Mus musculus

PROVIDER: GSE173982 | GEO | 2022/04/06

REPOSITORIES: GEO

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miR-138 controls interneuron function and short-term memory

Project description:miR-138 controls interneuron function and short-term memory

| PRJNA727797 | ENA

MicroRNA-138 controls hippocampal interneuron function and short-term memory in mice.

Project description:The proper development and function of neuronal circuits rely on a tightly regulated balance between excitatory and inhibitory (E/I) synaptic transmission, and disrupting this balance can cause neurodevelopmental disorders, for example, schizophrenia. MicroRNA-dependent gene regulation in pyramidal neurons is important for excitatory synaptic function and cognition, but its role in inhibitory interneurons is poorly understood. Here, we identify miR138-5p as a regulator of short-term memory and inhibitory synaptic transmission in the mouse hippocampus. Sponge-mediated miR138-5p inactivation specifically in mouse parvalbumin (PV)-expressing interneurons impairs spatial recognition memory and enhances GABAergic synaptic input onto pyramidal neurons. Cellular and behavioral phenotypes associated with miR138-5p inactivation are paralleled by an upregulation of the schizophrenia (SCZ)-associated Erbb4, which we validated as a direct miR138-5p target gene. Our findings suggest that miR138-5p is a critical regulator of PV interneuron function in mice, with implications for cognition and SCZ. More generally, they provide evidence that microRNAs orchestrate neural circuit development by fine-tuning both excitatory and inhibitory synaptic transmission.

| S-EPMC8963876 | biostudies-literature

Inhibition of microRNA-138 enhances bone formation in multiple myeloma bone marrow niche

Project description:Myeloma bone disease is a devastating complication of multiple myeloma (MM) and is caused by dysregulation of bone remodeling processes in the bone marrow microenvironment. Previous studies showed that microRNA-138 (miR-138) is a negative regulator of osteogenic differentiation of mesenchymal stromal cells (MSCs) and that inhibiting its function enhances bone formation in vitro. In this study, we explored the role of miR-138 in myeloma bone disease and evaluated the potential of systemically delivered locked nucleic acid (LNA)-modified anti-miR-138 oligonucleotides in suppressing myeloma bone disease. We showed that expression of miR-138 was significantly increased in MSCs from MM patients (MM-MSCs) and myeloma cells compared to those from healthy subjects. Furthermore, inhibition of miR-138 resulted in enhanced osteogenic differentiation of MM-MSCs in vitro and increased number of endosteal osteoblastic lineage cells (OBCs) and bone formation rate in mouse models of myeloma bone disease. RNA sequencing of the OBCs identified TRPS1 and SULF2 as potential miR-138 targets that were de-repressed in anti-miR-138 treated mice. In summary, these data indicate that inhibition of miR-138 enhances bone formation in MM and that pharmacological inhibition of miR-138 could represent a new therapeutic strategy for treatment of myeloma bone disease.

2018-06-01 | GSE111651 | GEO

Identification of the downstream target genes of miR-138 in gastric cancer

Project description:Our data showed that EIF4EBP1, NINJ1, CLIC3, STMN3, SPINK4, CD44, GSN, PRSS23 et al. were strongly downregulated by miR-138-mimics in gastric cancer (GC) cell lines. Besides, miR-138-5p has a profound effect on EMT signaling and proliferation signaling. In the EMT signaling, miR-138-5p negatively regulates the expression of SOX4, VIM, TGFB1, BMP1, ECM1 and CXCL8; In the cell proliferation signaling, miR-138-5p could negatively regulates the expression of PCNA, RHOC and CCND3.

2021-10-08 | GSE183654 | GEO

MicroRNA-138: A Pro-survival OncomiR for Glioma Stem Cells is Associated with Tumor Recurrence [mRNA]

Project description:We report the identification of microRNA-138 (miR-138), as a molecular signature of GSCs and demonstrate a vital role for miR-138 to promote growth and survival of bona fide tumor-initiating cells with self-renewal potential. Keywords: Expression profiling by array Total RNA from GSCs 5 days after transduction with lentivirus expressing anti-miR-138 or scrambled sequence was subjected to microarray analysis

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Identification of targets of miR-138 in Neuro-2a and 293T cells by RNAseq

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.

2020-04-27 | GSE127502 | GEO

MicroRNA-138: A Diagnostic Biomarker and Therapeutic Target for the Aggressive Basal-like subtype of Breast Cancer

Project description:This study identifies miR-138 as a prognostic biomarker for basal breast carcinoma. Identification of differentially regulated genes upon miR-138 knockdown (AntagomiR-138) in basal breast cancer cell lines MDA-MB-231

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MicroRNA-138: A Pro-survival OncomiR for Glioma Stem Cells is Associated with Tumor Recurrence [miRNA]

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Identification of viral and host targets of miR-138 by PAR-CLIP analysis of herpes simplex virus 2 infected 293T cells

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.

2021-11-01 | GSE155402 | GEO

Chd2 is necessary for neural circuit development and long-term memory

Project description:Considerable evidence suggests loss of function mutations in the chromatin remodeler, CHD2, contribute to a broad spectrum of human neurodevelopmental disorders. However, it is unknown how CHD2 mutations lead to impaired brain function. Here we report mice with heterozygous mutations in Chd2 exhibit deficits in neuron proliferation and a shift in neuronal excitability that included divergent changes in excitatory and inhibitory synaptic function. Further in vivo experiments show Chd2+/- mice displayed aberrant cortical rhythmogenesis and severe deficits in long-term memory, consistent with phenotypes observed in humans. We identified broad, age-dependent transcriptional changes in Chd2+/- mice, including alterations in neurogenesis, synaptic transmission and disease-related genes. Deficits in interneuron density and memory caused by Chd2+/- were reproduced by Chd2 mutation restricted to a subset of inhibitory neurons and corrected by interneuron transplantation. Our results provide initial insight into how Chd2 haploinsufficiency leads to aberrant cortical network function and impaired memory.

2018-10-18 | GSE112196 | GEO

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