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Transcriptome-based screening of ion channels and transporters in a migratory chondroprogenitor cell line isolated from late-stage osteoarthritic cartilage

ABSTRACT: Chondrogenic progenitor cells (CPCs) may be used as an alternative source of cells with potentially superior chondrogenic potential compared to mesenchymal stem cells (MSCs), and could be exploited for future regenerative therapies targeting articular cartilage in degenerative diseases such as osteoarthritis. We studied the profiles of those ion channel and transporter families that may be relevant to chondroprogenitor cell physiology using Affymetrix microarrays.

ORGANISM(S): Homo sapiens

PROVIDER: GSE160886 | GEO | 2021/12/31

REPOSITORIES: GEO

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Project description:Aging is a major risk factors for osteoarthritis (OA), and cartilage of the elder are more sensitive to mechanical loading stress. Recently, cartilage progenitor cells (CPCs) arose much interests due to its important role in maintaining cartilage homeostasis. However, the potential mechanism of increased sensitivity to mechanical stress in CPCs has not been elucidated. The aim of this study was to investigate the potential links between aging and age-related OA through establish CPCs replicative senescence model and fluid flow shear stress (FFSS) stimulated degeneration model. Small RNA and mRNA sequence were conducted to investigate miRNA-related mechanisms in this process. By gain-and-lost strategy we investigated the age-related miRNAs and their impacts on exacerbating the progression of biomechanical stimulated TMJ-OA. miR-708-5p was identified as age-related miRNA in CPCs, and TLR4 was identified as its direct target through luciferase report assay. Age-related miR-708-5p deficiency increased sensitivity of CPCs for exposure to FFSS by liberating TLR4 expression. Intra-articular delivery agomiR-708-5p alleviated TMJ osteoarthritic cartilage lesions in mice. In conclusion, age-related miR-708-5p deficiency increases the sensitivity to mechanical loading stress and promotes CPCs senescence like degeneration via TLR4.

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Enhancing the chondrogenic potential of chondrogenic progenitor cells by deletion of RAB5C

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A Chondrogenic Molecule that Repairs Cartilage by Transcriptional Regulation of CBF-beta

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Forward and reverse degradomics defines the proteolytic landscape of human knee osteoarthritic cartilage and the role of the serine protease HtrA1

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Genomic profile of transporters and ion channels

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A Chondrogenic Molecule that Repairs Cartilage by Transcriptional Regulation of CBF-beta

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Development of human cartilage circadian rhythm in a stem cell-chondrogenesis model

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