SARS-CoV-2 neurotropism induces anxiety/depression-like behaviors in mice [RNA-seq]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1213723 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32060500_1.fastq.gz | Fastqsanger.gz | |||
| SRR32060500_2.fastq.gz | Fastqsanger.gz | |||
| SRR32060492_1.fastq.gz | Fastqsanger.gz | |||
| SRR32060492_2.fastq.gz | Fastqsanger.gz | |||
| SRR32060493_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 18 |
Similar Datasets
Project description:The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has been linked to a wide range of neurological symptoms. In this study, the impact of SARS-CoV-2 infection on neuropsychiatric disorders in mice was investigated. To elucidate the role of SARS-CoV-2 infection in behavioral changes, we utilized a highly virulent mouse-adapted SARS-CoV-2 strain (SARS2-N501YMA30) to infect young C57BL/6 mice.
2025-01-25 | GSE287550 | GEO
Project description:Emerging evidence has shown that noncoding RNAs, particularly microRNAs (miRNAs), contribute to the pathogenesis of mood and anxiety disorders, although the molecular mechanisms are poorly understood. Here we show altered levels of miR-17-92 in adult hippocampal neural progenitors have a significant impact in neurogenesis and anxiety- and depression-related behaviors in mice. miR-17-92 deletion in adult neural progenitors causes a decrease, while its overexpression an increase of neurogenesis in the dentate gyrus, through regulating genes in the glucocorticoid pathway, especially serum- and glucocorticoid-inducible protein kinase-1 (Sgk1). miR-17-92 knockout mice show anxiety- and depression-like behaviors, whereas miR-17-92 overexpressing mice exhibit anxiolytic and antidepression-like behaviors. Furthermore, we show that miR-17-92 expression in the adult mouse hippocampus responds to chronic stress, and miR-17-92 rescues proliferation defects, induced by corticosterone, in hippocampal neural progenitors. Our study uncovers a crucial role for miR-17-92 in adult neural progenitors to regulate neurogenesis and anxiety- and depression-like behaviors.
2016-12-09 | GSE83636 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE290414 | GEO
Project description:Exploring the Mechanism of SETDB1 in Regulating Neuroinflammation and Anxiety-Depression-like Behaviors
| PRJNA1227981 | ENA
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275354 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275353 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275352 | GEO
Project description:Depression is a globally prevalent disabling mental illness with serious social hazards. Previous studies suggest that neuroinflammation plays an important role in the pathogenesis of depression, but the underlying mechanism remains elusive. Endogenous retrovirus (ERVs) is a type of transposable elements (TEs), consists around 8% of human genome but are mostly silenced in vivo. Repressive histone modifications H3K9me3 mediated by the methyltransferase SETDB1 plays a key role in maintaining silencing of ERVs. In this study, we constructed Setdb1-CK-cKO (KO) transgenic mice. Behavioral tests showed that the KO mice exhibited anxiety-depression-like behaviors compared to wild type (WT). Cortex snRNA-seq analysis revealed significant changes in astrocytes in addition to excitatory neurons, with the emergence of a new sub cluster of astrocytes in the KO whose transcriptional profile exhibited specific ERVs activation. We observed a large number of GFAP-positive cells in the KO cortex and striatum by Immunostaining, suggesting reactive astrogliosis. Transcriptomic analysis of astrocytes revealed significant upregulation of genes associated with inflammation in the KO cortex, including multiple chemokine genes. To investigate the potential molecular mechanism underlying "endogenous" neuroinflammation in KO mice, we focused on the purinergic receptor P2X7R, which has been reported to play an important role in mediating neuroinflammation and emotional behaviors. Most importantly, we found that the expression of P2rx7 was significantly upregulated in the KO neuron. We applied multiple epigenomic methods (RNA-seq, ATAC-seq, H3K9me3 ChIP-seq) to analyze in detail the molecular mechanism by which SETDB1 regulates the P2rx7 gene expression, and identified a novel enhancer fragment, mE1. We further constructed a SETDB1 knockout human 293T cell line and examined chromatin accessibility by ATAC-seq. We found a regulatory fragment hE1 with enhancer activity, which was present at a similar location in the human P2RX7 locus, suggesting that this mechanism is conserved between human and mouse. Knockout of P2X7R effectively ameliorated neuroinflammation and partially alleviated neuronal dysfunction as well as behaviors in Setdb1-CK-cKO mice.
2026-04-04 | GSE275351 | GEO
Project description:Investigating the molecular basis and correlates of anxiety-related and depression-like behaviors, we generated a mouse model consisting of high (HAB) and low (LAB) anxiety-related behavior mice. We utilized the elevated plus-maze for testing the genetic predisposition to anxiety-related behavior and, consequently, used this as selection criterion for the inbreeding of our animals. In depression-related tests, HAB mice display a more passive, depression-like coping strategy than LAB mice, resembling clinical comorbidity of anxiety and depression as observed in psychiatric patients. Using a microarray approach, the hypothalamic paraventricular nucleus (PVN), the basolateral/lateral (BLA), the medial (MeA) and central amygdala (CeA), the nucleus accumbens (NAc), the cingulate cortex (Cg) and the supraoptic nucleus (SON) – centers of the central nervous anxiety and fear circuitries – were investigated and screened for differences between HAB and LAB mice. Analysis was performed from six animals per line (HAB and LAB, respectively) pooled per brain region in ten technical replicates, thereof five with a dye-swapped design giving a total of 70 array slides analyzed. The LAB mouse line is referred to as reference.
2011-08-29 | E-GEOD-28999 | biostudies-arrayexpress
Project description:Exploring the Mechanism of SETDB1 in Regulating Neuroinflammation and Anxiety-Depression-like Behaviors [snRNA-seq]
| PRJNA1150524 | ENA