GEO series
cGAS-STING axis activation drove inflammatory phenotype acquisition of senescent nucleus pulposus cells via p65-mediated transcriptional modulation
GSE244403
Homo sapiens
Genome binding/occupancy profiling by high throughput sequencing
12 samples
Submitted 2024/03/20
Platform GPL24676
Summary
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.
Published in
Zhang W, Li G, Zhou X et al.
· The Journal of clinical investigation 2024
· PMID 38488012
· doi:10.1172/JCI165140
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE244403_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 12 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1022798 and SRA study SRP464016. Searching any of these in the dataset finder brings you back here.
Study design
12 conditions, each sampled once — no replicated groups
Read from 12 sample titles: 12 distinct titles with little repetition. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM7815488 Degenerated NP cells #1 for p65 CUT&Tag
- GSM7815489 Degenerated NP cells #2 for p65 CUT&Tag
- GSM7815490 Degenerated NP cells #3 for p65 CUT&Tag
- GSM7815491 No-degenerated NP cells #1 for p65 CUT&Tag
- GSM7815492 No-degenerated NP cells #2 for p65 CUT&Tag
- GSM7815493 No-degenerated NP cells #3 for p65 CUT&Tag
- GSM7815494 Senescent NP cells treated with DMSO #1 for p65 CUT&Tag
- GSM7815495 Senescent NP cells treated with DMSO #2 for p65 CUT&Tag
- GSM7815496 Senescent NP cells treated with DMSO #3 for p65 CUT&Tag
- GSM7815497 Senescent NP cells treated with H-151 #1 for p65 CUT&Tag
- GSM7815498 Senescent NP cells treated with H-151 #2 for p65 CUT&Tag
- GSM7815499 Senescent NP cells treated with H-151 #3 for p65 CUT&Tag
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