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HPIP controls osteoarthritis cartilage degeneration

ABSTRACT: HPIP controls osteoarthritis cartilage degeneration

PROVIDER: PRJNA391300 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5725510_1.fastq.gz	Fastqsanger.gz
	SRR5725510_2.fastq.gz	Fastqsanger.gz
	SRR5725511_1.fastq.gz	Fastqsanger.gz
	SRR5725511_2.fastq.gz	Fastqsanger.gz
	SRR5725512_1.fastq.gz	Fastqsanger.gz

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Project description:NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis

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HPIP controls osteoarthritis cartilage degeneration [RNA-seq]

Project description:To underly the potential downstream transcriptional regulation of HPIP that could account for cartilage and skeletal development. RNA-seq analysis were performed in HPIP knockout and control primary chondrocytes.Among the 1271 significantly differentially expressed genes, transcripts for 486 (7%) of them were upregulated while transcripts for 785 (11%) were downregulated in HPIP knockout chondrocytes compared to the controls. We found HPIP was closely correlated with the cartilage development.

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NG2/CSPG4 regulates cartilage degeneration during TMJ osteoarthritis

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Project description:Osteoarthritis (OA) is a serious degenerative joint disease with high morbidity and is currently incurable because of its poorly defined underlying molecular basis. Here, we demonstrated that Tiki2, a membrane-tethered proteolytic Wnt inhibitor, is highly expressed in the articular chondrocytes of hyaline cartilage and that its expression negatively correlates with osteoarthritis. Tiki2 haploinsufficiency in mice causes spontaneous articular cartilage degeneration. Tiki2 deletion in chondrocytes accelerates instability-induced knee joint osteoarthritis progression in mice. Mechanistically, Tiki2 antagonizes Wnt signaling in chondrocytes and maintains chondrocyte anabolic gene expression. Moreover, intra-articular administration of a TIKI2-expressing adeno-associated virus significantly alleviated OA progression in mice, and expressing TIKI2 promoted chondrogenesis and chondrocyte redifferentiation and inhibited hypertrophic differentiation in vitro. Our results reveal the function of Tiki2 in articular cartilage homeostasis and osteoarthritis and suggest that Tiki2 is a potential target for osteoarthritis therapy.

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