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CGAS-STING axis activation drove inflammatory phenotype acquisition of senescent nucleus pulposus cells via p65-mediated transcriptional modulation

ABSTRACT: cGAS-STING axis activation drove inflammatory phenotype acquisition of senescent nucleus pulposus cells via p65-mediated transcriptional modulation

PROVIDER: PRJNA1022798 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26243544_1.fastq.gz	Fastqsanger.gz
	SRR26243544_2.fastq.gz	Fastqsanger.gz
	SRR26243545_1.fastq.gz	Fastqsanger.gz
	SRR26243545_2.fastq.gz	Fastqsanger.gz
	SRR26243546_1.fastq.gz	Fastqsanger.gz

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cGAS-STING axis activation drove inflammatory phenotype acquisition of senescent nucleus pulposus cells via p65-mediated transcriptional modulation

Project description:Given the leading cause of disability worldwide, low back pain (LBP) is recognized as a pivotal socio-economic challenge to the aging population, which is importantly attributed to intervertebral disc degeneration (IVDD), a highly prevalent affliction of aging. Elastic nucleus pulposus (NP) tissue is essential for maintenance of IVD structural and functional integrity. Native NP cells exhibit crucial functions for regulating extracellular matrix homeostasis, constructing an accommodating biomechanical environment and maintaining the gelatinous property of NP tissue. The accumulation of senescent NP cells with inflammatory hypersecretory phenotype due to aging and other damaged factors is a distinctive hallmark of IVDD initiation and progression. In this study, we revealed a mechanism of IVDD progression in which aberrant genomic DNA damage promotes NP cell inflammatory senescence via activation of cGAS-STING axis. cGAS-STING axis activation drove inflammatory phenotype acquisition and inflammatory hypersensitivity to damaged signals of senescent NP cells via p65-mediated transcriptional modulation. And STING pharmacological inhibitor notably suppressed p65-mediated inflammatory response formation and senescence-associated screctory phenotype (SASP) acquisition of senescent cells.

2024-03-20 | GSE244403 | GEO

CytoDNA triggered NP cell inflammatory senescence via cGAS-STING axis sensing but not AIM2 inflammasome activation

Project description:Given the leading cause of disability worldwide, low back pain (LBP) is recognized as a pivotal socio-economic challenge to the aging population, which is importantly attributed to intervertebral disc degeneration (IVDD), a highly prevalent affliction of aging. Elastic nucleus pulposus (NP) tissue is essential for maintenance of IVD structural and functional integrity. Native NP cells exhibit crucial functions for regulating extracellular matrix homeostasis, constructing an accommodating biomechanical environment and maintaining the gelatinous property of NP tissue. The accumulation of senescent NP cells with inflammatory hypersecretory phenotype due to aging and other damaged factors is a distinctive hallmark of IVDD initiation and progression. In this study, we revealed a mechanism of IVDD progression in which aberrant genomic DNA damage promoted NP cell inflammatory senescence via activation of cGAS-STING axis. cGAS-STING axis activation drove inflammatory phenotype acquisition and inflammatory hypersensitivity to damaged signals of senescent NP cells via NF-ÎºB pathway-mediated transcriptional modulation. And the administration of H-151 revealed that STING pharmacological inhibitor notably suppressed the inflammatory response formation and senescence associated screctory phenotype (SASP) acquisition of senescent cells. Furthermore, blocking STING activation could suppress NF-ÎºB pathway-mediated transcriptional remodeling and inflammatory phenotype acquisition in senescent NP cells.

2024-03-20 | GSE245147 | GEO

p65

Project description:p65

| PRJNA811604 | ENA

cGAS maintains basal antiviral state

Project description:Upon recognition of aberrantly located DNA, the innate immune sensor cGAS activates STING/IRF-3-driven antiviral responses. Here we characterized the ability of a specific variant of the cGAS-encoding gene MB21D1, rs610913, to alter cGAS-mediated DNA sensing and viral infection. rs610913 is a frequent G>T polymorphism resulting in a P261H exchange in the cGAS protein. Data from the International Collaboration for the Genomics of HIV suggested that rs610913 nominally associates with HIV-1 acquisition in vivo. Molecular modeling of cGAS(P261H) hinted towards the possibility for an additional binding site for a potential cellular co-factor in cGAS dimers. However, cGAS(WT) or cGAS(P261H)-reconstituted THP-1 cGAS KO cells shared steady-state expression of interferon-stimulated genes (ISGs), as opposed to cells expressing the enzymatically inactive cGAS(G212A/S213A). Accordingly, cGAS(WT) and cGAS(P261H) cells were less susceptible to lentiviral transduction and infection with HIV-1, HSV-1, and Chikungunya virus as compared to cGAS KO- or cGAS(G212A/S213A) cells. Upon DNA challenge, innate immune activation appeared to be mildly reduced upon expression of cGAS(P261H) compared to cGAS(WT). Finally, DNA challenge of PBMCs from donors homozygously expressing rs610913 provoked a trend towards a slightly reduced type I IFN response as compared to PBMCs from GG donors. Taken together, the steady-state activity of cGAS maintains a base-line antiviral state rendering cells more refractory to ISG-sensitive viral infections. rs610913 failed to grossly differ phenotypically from the wild-type gene, suggesting that cGAS(P261H) and wild-type cGAS share a similar ability to sense viral infections in vivo.

2022-05-25 | GSE203334 | GEO

Me-RIP- Sequencing Analysis of normal and senescent nucleus pulposus cells Transcriptomes

Project description:N6-methyladenosine (m6A) is the most prevalent modification of eukaryotic cells st post-transcriptional level. The goals of this study are to compare the N6-methyladenosine modification of transcripts in normal and senescent nucleus pulposus cells using Me-RIP-seq

2022-03-23 | GSE169484 | GEO

Expression data from synovium, bone marrow and nucleus pulposus

Project description:Synovial and bone marrow mesenchymal stem cells after intradiscally injection show regenerative effects of nucleus pulposus. Microarray analyses of rats were performed to investigate the closeness of the gene profiles between the nucleus pulposus cells and the synovial or bone marrow mesenchymal stem cells. To investigate interaction between synovial mesenchymal stem cells and nucleus pulposus cells, human synovial mesenchymal stem cells and rat nucleus pulposus cells were co-cultured, and species specific microarray were performed. Synovium of knee joints, bone marrow and nucleus pulposus were harvested from rat or human, and cells were isolated for RNA extraction and hybridization on Affymetrix microarrays. To compare the gene profiles each other, isolated cells were mono-cultured respectively, and human synovial mesenchymal stem cells and rat nucleus pulposus cells were co-cultured.

2010-10-11 | E-GEOD-24612 | biostudies-arrayexpress

Gene induction in STAT1-/- fibroblasts transduced with lentiviruses expressing human cGAS

Project description:The hypothesis tested was that lentiviral driven cGAS expression activates antiviral gene expression. Cells were transduced with lentiviruses expressing cGAS or a control (firefly luciferase). Total RNA was harvested 48 h post-transduction and processed for Illumina BeadArray.

2013-12-01 | E-GEOD-52241 | biostudies-arrayexpress

MicroRNAs expression profiling of human nucleus pulposus cells: control vs. degeneration

Project description:MicroRNAs expression profiling of human nucleus pulposus cells derived from patients with disc degeneration in comparison with those derived from patients with scoliosis as control. Two-condition experiment: control nucleus pulposus cells vs. degenerative nucleus pulposus cells. Biological replicates: 3 control, 3 degenerated, independently harvested. Four replicates per array. The supplementary file 'GSE19943_fold_pvalue.txt' contains fold-changes and p-values.

2012-01-01 | E-GEOD-19943 | biostudies-arrayexpress

Examining changes in the chromosomal interaction network in replicative senescent, rapamycin treatment, and p65 inhibition

Project description:Analysis of HiC genome wide chromosomal interaction data in the context of replicative senescence, rapamycin treatment, the withdrawal of rapamycin, and with p65 inhibition in rapamycin withdrawal. This was done in order to determine what changes in chromosomal architecture occur during replicative senescence, and what impact rapamycin treatment or withdrawal or p65 inhibition has upon these changes.

2025-05-30 | GSE146584 | GEO

RNA-binding proteins hnRNPM and ELAVL1 promote type-I interferon induction downstream of the nucleic acid sensors cGAS and RIG-I

Project description:RIG-I like helicases (RLHs) and cGAS are crucial cytosolic sensors of viral RNA and DNA, respectively, and induce type I IFNs via TBK1/IKKε. hnRNPM was described to possess antimicrobial activities. Here, we show that hnRNPM promotes IRF3 phosphorylation and type I IFN induction downstream of cGAS and RIG-I in THP-1 cells and primary human fibroblasts. Interactome analysis revealed that hnRNPM forms a multiprotein complex with ELAVL1, TBK1, IKKε, IKKβ, and NF-κB p65. hnRNPM, ELAVL1, and TBK1 predominantly interacted in the cytosol. To our knowledge, hnRNPM and ELAVL1 represent the first non-redundant signaling components merging the cGAS-STING and RIG-I–MAVS pathways. Therefore, our findings may have implications for host defense and auto-inflammatory diseases.

2024-11-11 | PXD028160 | Pride

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