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Genome-wide DNA methylation profile analysis of human intervertebral disc degeneration

ABSTRACT: Genome-wide DNA methylation profile analysis of human intervertebral disc degeneration

PROVIDER: PRJNA532833 | ENA |

REPOSITORIES: ENA

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Intervertebral disc degeneration

Project description:Intervertebral disc degeneration

| PRJNA962588 | ENA

Genome-wide DNA methylation profile analysis of human intervertebral disc degeneration

Project description:The pathophysiology of intervertebral disc (IVD) degeneration is not entirely understood; however, environmental and endogenous factors under genetic predisposition are considered to initiate the degenerative changes of human IVDs. Aberrant epigenetic alterations play a pivotal role in several diseases, including osteoarthritis. However, epigenetic alternations, including DNA methylation, in IVD degeneration have not been evaluated. The purpose of this study was to comprehensively compare the genome-wide DNA methylation profiles of human IVD tissues, specifically nucleus pulpous (NP) tissues, with early and advanced stages of disc degeneration. We conducted, for the first time, a genome-wide DNA methylation profile comparative study and observed significant differences in DNA methylation profiles between early and advanced stages of human IVD degeneration. The overview of the DNA methylation profile in the current study revealed that differentially methylated loci were identified in many genes associated with known molecules that have been reported to be relevant to IVD degeneration. Importantly, changes in DNA methylation profiles were also found in genes that regulate the major signaling pathways, such as NF-κB, MAPK, and Wnt signaling, that are well known to be responsible for the pathogenesis of human disc degeneration.

2019-10-01 | GSE129789 | GEO

Proteomics for patients with intervertebral disc degeneration

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2024-04-10 | PXD051351 |

Nucleus pulposus related lncRNA and mRNA expression profiles in intervertebral disc degeneration

Project description:Intervertebral disc degeneration (IDD) leads to low back pain and disability globally. The pathophysiology of IDD is not entirely understood. There is increasing evidence that long noncoding RNAs (lncRNAs) play a key regulatory role in a wide range of biological processes. The purpose of this study was to comprehensively lncRNA and mRNA expression profiles of human intervertebral disc (IVD) tissues, specifically nucleus pulpous (NP) tissues, with early and advanced stages of disc degeneration. The overview of lncRNA and mRNA expression profiles in the current study revealed that differentially expressed lncRNAs and mRNAs were identified that have been reported to be relevant to IDD. Importantly, differentially expressed lncRNAs and mRNAs that regulate the major signaling pathways, such as NF-κB, MAPK, and Wnt signaling, that are well known to be responsible for the pathogenesis of IDD.

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HO1 activates autophagy to protect intervertebral disc degeneration

Project description:HO1 activates autophagy to protect intervertebral disc degeneration

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SIRT6 loss causes intervertebral disc degeneration in mice by dysregulating senescence and SASP status

Project description:Transcriptional analysis of 24-month-old primary nucleus pulposus (NP) and annulus fibrosus (AF) mouse disc tissues from Sirt6fl/fl and Sirt6cKO mice, which harbor a mutation which constiuitively deletes Sirtuin 6 in aggrecan expressing cells. SIRT6 loss causes intervertebral disc degeneration in mice by dysregulating senescence and SASP status

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Long-term treatment with senolytic drugs Dasatinib and Quercetin ameliorates age-dependent intervertebral disc degeneration in mice

Project description:Intervertebral disc degeneration is highly prevalent in the elderly population and is a leading cause of chronic back pain and disability. Studies have linked degenration with increased disc cell senescence. Likewise, senolytics such as Dasatinib + Quercetin combination may provide a novel approach to mitigate age-dependnt disc degeneration. We used microarrays to explore the transcriptomics of differentially expressed genes between aged disc compartments: AF vs NP at 23M, AF: D+Q vs Veh and NP: D+Q vs Veh.

2021-07-01 | GSE154619 | GEO

Single-cell sequencing reveals cellular heterogeneity of nucleus pulposus in intervertebral disc degeneration

Project description:Nucleus pulposus (NP) plays a vital role in intervertebral disc degeneration (IVDD). Previous studies have revealed cellular heterogeneity in the NP tissue during IVDD progression. Here, we used single cell RNA sequencing (scRNA-seq) to analyze the cellular and molecular alterations of diverse cell clusters during IVDD.

2024-11-14 | GSE251686 | GEO

TonEBP-deficiency accelerates age-dependent intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression

Project description:Our studies show that TonEBP-deficiency causes pronounced degeneration of all three intervertebral disc compartments with greater incidence of herniation in the mouse. The disc phenotype is marked by extracellular matrix remodeling, actin cytoskeleton rearrangements, and suppressed proinflammatory gene expression, advancing our understanding of the contributions of TonEBP in intervertebral disc homeostasis and disease. We used microarray to explore the transcriptomics of differentially expressed genes of annulus fibrosus (AF) and nucleus pulposus (NP) tissue in TonEBP haploinsufficient mice on a C57BL/6 background.

2021-08-05 | GSE135270 | GEO

Intervertebral disc degeneration, a loose definition for a more complex pathology? Insights from aging inbred mouse strains

Project description:Intervertebral disc degeneration is an important contributor to chronic low back pain. While a wide spectrum of clinically relevant degenerative disc phenotypes have been observed during aging, their molecular underpinning have not been established. We used microarrays to explore the transcriptomics of differentially expressed genes during aging (6M to 23M) in two strains: C57BL/6 and LG/J.

2020-06-08 | GSE134955 | GEO

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