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The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3

ABSTRACT: The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3

PROVIDER: PRJNA1149744 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30295788.fastq.gz	Fastqsanger.gz
	SRR30295789.fastq.gz	Fastqsanger.gz
	SRR30295790.fastq.gz	Fastqsanger.gz
	SRR30295791.fastq.gz	Fastqsanger.gz
	SRR30295792.fastq.gz	Fastqsanger.gz

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The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3

Project description:Aging is linked to a decline in cognitive functions and significantly increases the risk of neurodegenerative diseases. While molecular changes in all central nervous system (CNS) cell types contribute to aging-related cognitive decline, the mechanisms driving disease development or offering protection remain poorly understood. Long non-coding RNAs (lncRNAs) have emerged as key regulators of cellular functions and gene expression, yet their roles in aging, particularly within glial cells, are not well characterized. In this study, we investigated lncRNA expression profiles in non-neuronal cells from aged mice. We identified 3222401L13Rik, a previously unstudied lncRNA enriched in glial cells, as being specifically upregulated in astrocytes during aging. Knockdown of 3222401L13Rik in primary astrocytes revealed its critical role in regulating genes essential for neuronal support and synapse organization. This function was also conserved in human iPSC-derived astrocytes. Additionally, we found that 3222401L13Rik mediates its cellular effects through interaction with the transcription factor Neuronal PAS Domain Protein 3 (Npas3), and that overexpression of Npas3 effectively rescued the functional deficits observed in astrocytes lacking 3222401L13Rik. Our findings suggest that upregulation of 3222401L13Rik in aging astrocytes acts as a compensatory mechanism to enhance neuronal and synaptic support, potentially delaying the onset of molecular and structural changes in both astrocytes and neurons. Strategies to boost 3222401L13Rik expression earlier in life may help mitigate age-associated loss of neuronal plasticity.

2025-01-06 | GSE275168 | GEO

The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3 [young]

2026-01-12 | GSE286099 | GEO

The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3 [young]

Project description:The LncRNA 3222401L13Rik Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3 [young]

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Identification of NPAS3 cistrome in the mouse cortical astrocytes (DIV 14).

Project description:Genome-wide binding sites of NPAS3 were identified in mouse cortical astrocytes (DIV 14).

2022-07-19 | GSE179592 | GEO

NPAS3-regulated astrocyte mitochondria bioenergetics is required for cognition

Project description:The basic helix-loop-helix (bHLH) transcription factor neuronal PAS domain protein 3 (NPAS3) provides transcriptional regulation of metabolic pathways, and despite its name is highly expressed in astrocytes. NPAS3 variants have been associated with cognitive dysfunction in several neuropsychiatric conditions, but the underlying brain cell type-specific mechanisms remain obscure. Here, we report that NPAS3 is a key regulator of mitochondria bioenergetics in astrocytes. Selective deletion of Npas3 in mature murine astrocytes decreases expression of Slc25a18 and its protein product, mitochondrial glutamate carrier 2, leading to reduced oxidative phosphorylation and lactate production in astrocytes. This deficit subsequently causes reduced excitability, dendritic spine density, and dendritic arborization of medial prefrontal cortex pyramidal neurons. Mice with Npas3-deficient cortical astrocytes exhibit impaired trace fear conditioning, which is rescued by lactate treatment. Thus, the present study demonstrates a mechanistic link between NPAS3-dependent astrocyte mitochondria bioenergetics and cognitive function and provides insights for glia-targeting treatment of cognitive dysfunction in neuropsychiatric disease.

2026-05-04 | GSE274921 | GEO

LncRNA <i>3222401L13Rik</i> Is Upregulated in Aging Astrocytes and Regulates Neuronal Support Function Through Interaction with Npas3.

Project description: Not available

| S-EPMC11755665 | biostudies-literature

Identification of NPAS3 cistrome in the mouse cortical astrocytes (DIV 14).

Project description:Identification of NPAS3 cistrome in the mouse cortical astrocytes (DIV 14).

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Whole transcriptome sequencing of mouse cortical astrocytes (DIV 14).

Project description:To gain futher insight into the Npas3 regulatory network in astrocytes, RNA-seq was used to analyze the genome-wide changes resulting from the days in vitro (DIV) 14 astrocytes of P0 wild-type (WT) mice and littermate NPAS3-/- mice. Total RNA was extracted from DIV 14 astrocytes of P0 Npas3-/- and WT mice. Then, total RNA was quantiﬁed and quality controlled by Agilent Bioanalyzer 2100 system. After cDNA library construction, the library preparations were sequenced on an Illumina NovaSeq 6000 platform in Novogene.

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NPAS3-HEK293-standardcond-Illumina

Project description:NPAS3 or truncated NPAS3 overexpressed HEK293 cells or control HEK293 cells were collected at 24 hours after gene overexpression.Total RNA from alll samples was extracted.Biotinylated cRNA was prepared using the Illumina total Prep RNA application Kits.Hybridization, washing and scanning were performed according to the Illumina BeadStation 500* manual (revision C)

2011-10-03 | E-TABM-1078 | biostudies-arrayexpress

Whole transcriptome sequencing of Npas3+/- and WT cortex at P0 stage

Project description:Purpose: To gain insight into the impact of NPAS3 deficiency on astrogenesis in mice, RNA-seq was used to analyze the genome-wide changes resulting from Npas3+/- and WT cortex at P0 stage. Methods: Total RNA was extracted from Npas3+/- and WT cortex at P0 stage. Then, total RNA was quantified and quality controlled by Agilent Bioanalyzer 2100 system. After cDNA library construction, the library preparations were sequenced on an Illumina NovaSeq 6000 platform in Novogene. Results: At significance cutoffs corresponding to FDR < 0.05, a total of 625 DEGs were identified in Npas3+/- mice. Conclusions: Our results show that Npas3+/- mice exhibit defective astrogenesis and abnormal synapse function.

2022-07-19 | GSE179608 | GEO

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