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MicroRNA-132 regulates gene expression programs involved in microglial homeostasis

ABSTRACT: microRNA-132 regulates gene expression programs involved in microglial homeostasis

PROVIDER: PRJNA958254 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24258400_1.fastq.gz	Fastqsanger.gz
	SRR24258400_2.fastq.gz	Fastqsanger.gz
	SRR24258401_1.fastq.gz	Fastqsanger.gz
	SRR24258401_2.fastq.gz	Fastqsanger.gz
	SRR24258402_1.fastq.gz	Fastqsanger.gz

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microRNA-132 regulates gene expression programs involved in microglial homeostasis

Project description:microRNA-132 (miR-132), a known neuronal regulator, is one of the most robustly downregulated microRNAs (miRNAs) in the brain of Alzheimer’s disease (AD) patients. Increasing miR-132 in AD mouse brain ameliorates amyloid and Tau pathologies, and also restores adult hippocampal neurogenesis and memory deficits. However, the functional pleiotropy of miRNAs requires in-depth analysis of the effects of miR-132 supplementation before it can be moved forward for AD therapy. We employ here miR-132 loss- and gain-of-function approaches using single-cell transcriptomics, proteomics and in silico AGO-CLIP datasets to identify molecular pathways targeted by miR-132 in mouse hippocampus. We find that miR-132 modulation significantly affects the transition of microglia from a disease-associated to a homeostatic cell state. We confirm the regulatory role of miR-132 in shifting microglial cell states using human microglial cultures derived from induced pluripotent stem cells.

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RNA sequencing - Microglial A20 is a critical gatekeeper of CNS homeostasis

Project description:The goal of this study is to elucidate the role of microglial A20 in maintaining brain homeostasis, comparing fully deficient to partially deficient microglia tissue

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Microglial homeostasis requires balanced CSF-1/CSF-2 receptor signaling

Project description:Microglial homeostasis requires balanced CSF-1/CSF-2 receptor signaling

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Functional Involvement of Septal miR-132 in Extinction and Oxytocin-mediated Reversal of Social Fear

Project description:Social interactions are critical components for the survival of mammalian biology and evolution. Dysregulation of social behavior often leads to psychopathologies such as social anxiety disorder, which is characterized by an intense fear and avoidance of social situations. Using the social fear conditioning (SFC) paradigm, we analyzed expression levels of miR-132-3p and miR-124-3p within the septum, a brain region essential for social behavior and fear, after acquisition and extinction of social fear. Functional in vivo approaches using pharmacology, functional inhibition of miR-132-3p, viral miR-132 overexpression and shRNA-mediated knockdown of miR-132-3p within oxytocin receptor positive neurons confirmed septal miR-132-3p to be involved in social fear extinction and the oxytocin-mediated reversal of social fear. Moreover, Argonaute-RNA-co-immunoprecipitation-microarray analysis and further target mRNA quantification, depicted growth differentiation factor-5 (GDF-5) to be involved in miR-132-3p-mediated regulation of social fear extinction. Local application of GDF-5 resulted in impaired social fear extinction, an effect which seems to be mediated by miR-132-3p. In summary, we show that septal miR-132-3p is functionally involved in social fear extinction learning and oxytocin-mediated reversal of social fear.

2023-11-08 | GSE211449 | GEO

Therapeutic miR-132 inhibition reverses heart failure

Project description:Despite some success of pharmacotherapies targeting primarily neurohormonal dysregulation, heart failure is a growing global pandemic with increasing burden. Treatments that improve the disease by reversing heart failure at the cardiomyocyte level are lacking. MicroRNAs (miRNA) are transcriptional regulators of gene expression, acting through complex biological networks, and playing thereby essential roles in disease progression. Adverse structural remodelling of the left ventricle due to myocardial infarction (MI) is a common pathological feature leading to heart failure. We previously demonstrated increased cardiomyocyte expression of the miR-212/132 family during pathological cardiac conditions. Transgenic mice overexpressing the miR-212/132 cluster (miR-212/132-TG) develop pathological cardiac remodelling and die prematurely from progressive HF. Using both knockout and antisense strategies, we have shown miR-132 to be both necessary and sufficient to drive the pathological growth of cardiomyocytes in a murine model of left ventricular pressure overload. Based on the findings, we proposed that miR-132 may serve as a therapeutic target in heart failure therapy. Here we provide novel mechanistic insight and translational evidence for the therapeutic efficacy in small and large animal models (n=135) of heart failure. We demonstrate strong PK/PD relationship, dose-dependent efficacy and high clinical potential of a novel optimized synthetic locked nucleic acid phosphorothioate backbone antisense oligonucleotide inhibitor of miR-132 (antimiR-132) as a next-generation heart failure therapeutic.

2020-01-09 | PXD015337 | Pride

RNA sequencing - Microglial A20 is a critical gatekeeper of CNS homeostasis

Project description:RNA sequencing - Microglial A20 is a critical gatekeeper of CNS homeostasis

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Cannabinoid receptor 2 is necessary to induce toll-like receptor-mediated microglial activation.

Project description:The tight regulation of microglia activity is key for precise responses to potential threats, while uncontrolled and exacerbated microglial activity is neurotoxic. Microglial toll-like receptors (TLRs) are indispensable for sensing different types of assaults and triggering an innate immune response. Cannabinoid receptor 2 (CB2) signaling is a key pathway to control microglial homeostasis and activation, and its activation is connected to changes in microglial activity. We aimed to investigate how CB2 signaling impacts TLR-mediated microglial activation. Here, we demonstrate that deletion of CB2 causes a dampened transcriptional response to prototypic TLR ligands in microglia. Loss of CB2 results in distinct microglial gene expression profiles, morphology, and activation. We show that the CB2-mediated attenuation of TLR-induced microglial activation is p38 MAPK-dependent. Taken together, we demonstrate that CB2 expression and signaling are necessary to fine-tune TLR-induced activation programs in microglia.

2021-08-23 | GSE173337 | GEO

NACC2 is a molecular effector of miR-132 regulation at the interface between adult neurogenesis and Alzheimer’s disease

Project description:The process of generating new neurons at the hippocampal neurogenic niche, also referred to as adult hippocampal neurogenesis (AHN), is impaired in Alzheimer’s disease (AD). MicroRNA-132 (miR-132), the most consistently downregulated microRNA (miRNA) in AD, was recently identified as a potent regulator of AHN, exerting multilayered proneurogenic effects in adult neural stem cells (NSCs) and their progeny. Supplementing miR-132 in AD mouse brain restores AHN and relevant memory deficits, yet the exact mechanisms involved are still unknown. Here, we identify NACC2 as a novel miR-132 target implicated in both AHN and AD. miR-132 deficiency in mouse hippocampus induces Nacc2 expression and inflammatory signaling in adult NSCs. We show that miR-132-dependent regulation of NACC2 is involved in the initial stages of human NSC differentiation towards astrocytes and neurons. Later, NACC2 function in astrocytic maturation becomes uncoupled from miR-132. We demonstrate that NACC2 is present in reactive astrocytes surrounding amyloid plaques in mouse and human AD hippocampus, and that there is an anticorrelation between miR-132 and NACC2 levels in AD and upon induction of inflammation. Unraveling the molecular mechanisms by which miR-132 regulates neurogenesis and cellular reactivity in AD, will provide valuable insights towards its possible application as a therapeutic target.

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A global transcriptome analysis of keratinocytes upon overexpression of microRNA-132

Project description:MiR-132 is one of the most upregulated miRNAs in keratinocytes of human skin wounds during the inflammatory phase of healing; however its biological role during skin wound healing has not been studied. To study the genes regulated by miR-132, we transfected miR-132 mimics (pre-miR-132) into primary human keratinocytes to overexpress miR-132. We performed a global transcriptome analysis of keratinocytes upon overexpression of miR-132 using Affymetrix arrays.

2014-12-30 | GSE61139 | GEO

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