Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA268036 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The expression profiling of circular RNAs (circRNA) in human intervertebral disc degeneration (IDD)
| PRJNA280274 | ENA
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.
2023-02-09 | GSE186542 | GEO
Project description:IDD (Intervertebral disc degeneration) is an important cause of low back pain which has become a global public health problem. We aimed to determine the role of glutamine in the development of IDD and evaluate its mechanism to prevent IDD.
2024-03-20 | GSE226186 | GEO
Project description:Intervertebral disc degeneration (IDD) is an important cause of low back pain. And abnormal mechanical factors are an important contributor to IDD. To identify mechanical responsive miRNAs in IDD, we used a custom-made compression device to establish IDD in rats and considered as IDD group, and the Sham group was inserted with K-wires into coccyxes only. After four weeks, rat nucleus pulposus tissues were obtained for miR-seq analysis.
2024-06-20 | GSE230509 | GEO
Project description:ABSTRACT:
Intervertebral disc degeneration (IDD) arises from an intricate imbalance between the anabolic and catabolic processes governing the extracellular matrix (ECM) within the disc. Biochemical processes are complex, redundant and feedback-looped, and improved integration of knowledge is needed. To addess this, a literature-based regulatory network model (RNM) for nucleus pulposus cells (NPC) is proposed, representing the normal state of the intervertebral disc (IVD), in which proteins are represented by nodes that interact among each other through activation and/or inhibition edges. This model includes 32 different proteins and 150 edges by incorporating critical biochemical interactions in IVD regulation, tested in vivo or vitro in humans’ and animals’ NPC, alongside non tissue specific protein-protein interactions. We used the network to calculate the dynamic regulation of each node through a semi-quantitative method. The basal steady state successfully represented the activity of a normal NPC, and the model was assessed through the published literature, by replicating two independent experimental studies in human normal NPC. Pro-catabolic or pro-anabolic shifts of the network activated by nodal perturbations could be predicted. Sensitivity analysis underscores the significant influence of transforming growth factor beta (TGF-β) and interleukin-1 receptor antagonist (IL-1Ra) on the regulation of structural proteins and degrading enzymes within the system. Given the ongoing challenge of elucidating the mechanisms driving ECM degradation in IDD, this unique IVD RNM holds promise as a tool for exploring and predicting IDD progression, shedding light on IVD phenotypes and guiding experimental research efforts.
2024-11-04 | MODEL2407080001 | BioModels
Project description:Understanding the molecular mechanisms regulating the maintenance and destruction of intervertebral disc may lead to the development of new therapies for intervertebral disc degeneration (IDD). Here we present evidence from miRNA microarray analyses of clinical data sets along with in vitro and in vivo experiments that miR-141 is a key regulator of IDD. Gain- and loss-of-function studies show that miR-141 drives IDD by inducing nucleus pulposus (NP) apoptosis. Furthermore, miR-141 KO in mice attenuated spontaneous and surgically induced IDD. Mechanistically, miR-141 promotes IDD development by targeting and depleting SIRT1, a negative regulator of NF-κB pathway. Therapeutically, upregulation or downregulation of miR-141 by nanoparticle delivery in IDD model aggravated or alleviated experimental IDD, respectively. Our findings reveal a novel mechanism by which miR-141, in part, promotes IDD progression by interacting with SIRT1/NF-κB pathway. Blockade of miR-141 in vivo may serve as a potential therapeutic approach in the treatment of IDD.
2018-12-11 | GSE116726 | GEO
Project description:Dysregulation of microRNAs (miRNAs) plays a critical role in the development of intervertebral disc degeneration (IDD). In this study, we present evidence from in vitro and in vivo research to elucidate the mechanism underlying the role of miR-760 in IDD. miRNA microarray and quantitative reverse transcription-polymerase chain reaction were used to determine the miRNA profiles in patients with IDD. Functional analysis was performed to evaluate the role of miR-760 in the pathogenesis of IDD. Luciferase reporter and western blotting assays were used to confirm the miRNA targets. The expression of miR-760 was significantly decreased in degenerative nucleus pulposus (NP) cells and negatively correlated with disc degeneration grade. Functional assays demonstrated that miR-760 delivery significantly increased NP cell proliferation and promoted the expression of collagen II and aggrecan. Moreover, MyD88 was identified as a target gene of miR-760. miR-760 effectively suppressed MyD88 expression by interacting with the 3′-untranslated region, which was abolished by miR-760 binding site mutations. An in vivo experiment using an IDD mouse model showed that the upregulation of miR-760 could effectively suspend IDD. Therefore, miR-760 was found to play an important role in IDD and can be used as a promising therapeutic target for the treatment of patients with IDD.
2022-03-17 | E-MTAB-11554 | biostudies-arrayexpress
Project description:Intervertebral disc degeneration (IDD) results from dysfunction of nucleus pulposus cells (NPs) and exhaustion of NP progenitors (ProNPs). Cellular applications of NPs during IDD are currently limited by lack of in vivo studies showing whether NPs are heterogenous and contain ProNPs throughout postnatal stages. Here, using single-cell RNA sequencing of purified NPs, we mapped four molecularly defined populations and identified Urotensin II receptor (UTS2R)-expressing postnatal ProNPs, which markedly exhausted during IDD, in mouse and human specimens. Lineage tracing showed that UTS2R+ ProNPs preferentially reside in the NP periphery with its niche factor-Tenascin-C and give rise to functional NPs. We also demonstrate that transplanting UTS2R+ ProNPs with Tenascin-C to injured intervertebral discs attenuates the progression of IDD. Our findings provide a novel NP cell atlas, identify resident ProNPs with regenerative potential and reveal promising diagnostic and therapeutic targets for IDD.
2024-12-30 | GSE192789 | GEO
Project description:Intervertebral disc degeneration
| PRJNA962588 | ENA
Project description:Intervertebral disc degeneration (IDD) is a major cause of low back pain (LBP), and the pathogenesis remains unknown. Recently, an autoregulating circadian rhythm was identified in intervertebral discs (IVDs), the abolition of which led to IDD. The genetic disruption of the mouse IVD molecular clock, specifically through the disruption of Bmal1, predisposes mice to IDD. However, the precise role of circadian gene Bmal1 in IDD remain elusive. Using a tandem mass tag (TMT)-based quantitative proteomics approach, we characterized the proteomes and phosphoproteomes of rat nucleus pulposus cells (NPCs) treated with Bmal1 shRNA or its negative control lentivirus.
2021-10-21 | PXD029273 |