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Chondrocytes differentiation and immune cells interactions of Endplate Cells in Human Intervertebral Disc Degeneration

ABSTRACT: Chondrocytes differentiation and immune cells interactions of Endplate Cells in Human Intervertebral Disc Degeneration

PROVIDER: PRJNA1076495 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27966812_1.fastq.gz	Fastqsanger.gz
	SRR27966812_2.fastq.gz	Fastqsanger.gz
	SRR27966813_1.fastq.gz	Fastqsanger.gz
	SRR27966813_2.fastq.gz	Fastqsanger.gz
	SRR27966814_1.fastq.gz	Fastqsanger.gz

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Chondrocytes differentiation and immune cells interactions of Endplate Cells in Human Intervertebral Disc Degeneration

Project description:We performed the single-cell RNA-sequencing analysis (scRNA-seq) of the cells focusing on degenerative human endplates. By unsupervised clustering of the 8,534 single-cell based on the gene expression, we identified nine distinct cell types. We employed Gene ontology (GO) analysis, Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis, and the single-cell regulatory network inference and clustering (SCENIC) to determine the enriched pathways and transcriptional activities across seven chondrocyte subpopulations. Furthermore, two cell fates of chondrocyte differentiation were found by trajectory analysis, one was enriched in inflammation-related genes, and the other was related to extracellular matrix (ECM). Additionally, the intercellular interactions of MAs and chondrocytes, T/NK cells and chondrocytes were examined by ligand-receptor pairs analysis, showing the important regulative function of FN1 from MAs and CD74 from T/NK cells during endplate degeneration.

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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.

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Project description:Despite the high prevalence of age-dependent intervertebral disc calcification, there is a glaring lack of treatment options for this debilitating pathology. Here, we investigate the efficacy of long-term oral K3Citrate supplementation in ameliorating disc calcification in LG/J mice, a model of spontaneous age-associated disc calcification. K3Citrate successfully reduced the incidence of disc calcification in LG/J mice without deleterious effects on vertebral bone structure, plasma chemistry, and locomotion. Notably, a positive effect on grip strength, a marker of frailty, was evident in treated mice. Spectroscopic investigation of the persisting calcified nodules indicated K3Citrate did not alter the mineral composition, and collagen 10 and aggrecan staining revealed that reactivation of an endochondral differentiation program in endplates may drive LG/J disc calcification. Importantly, K3Citrate reduced calcification incidence without altering the abundance of endplate hypertrophic chondrocytes, suggesting mitigation of disc calcification through Ca2+ chelation. This was further supported by the inability of K3Citrate to inhibit hypertrophic differentiation of chondrogenic ATDC5 cells and minimal effects on their metabolic status. Overall, this study sheds light on the pathogenesis of intervertebral disc calcification in LG/J mice and underscores the therapeutic potential of K3Citrate as a systemic intervention strategy for disc calcification.

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