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Identification of the key epigenetic determinants of chondrocyte aging in humans (ATAC-seq)

ABSTRACT: Identification of the key epigenetic determinants of chondrocyte aging in humans (ATAC-seq)

PROVIDER: PRJNA751606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15328205.fastq.gz	Fastqsanger.gz
	SRR15328206.fastq.gz	Fastqsanger.gz
	SRR15328207.fastq.gz	Fastqsanger.gz

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Identification of the key epigenetic determinants of chondrocyte aging in humans

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Identification of the key epigenetic determinants of chondrocyte aging in humans (Cut&Run)

Project description:Articular chondrocytes undergo functional changes and their regenerative potential declines with age. Although the molecular mechanisms guiding articular cartilage aging is poorly understood, DNA methylation is known to play a mechanistic role in aging. However, our understanding of DNA methylation in chondrocyte development across human ontogeny is limited. To better understand DNA methylome changes, methylation profiling was performed in human chondrocytes. This study reveals association between methylation of specific CpG sites and chondrocyte age. We also determined the putative binding targets of STAT3, a key age-patterned TF in fetal chondrocytes and genetic ablation of STAT3 induced a global genomic hypermethylation. Moreover, an epigenetic clock built for adult human chondrocytes revealed that exposure of aged adult human chondrocytes to STAT3 agonist, decreased epigenetic age. Taken together, this work will serve as a foundation to understand development and aging of chondrocytes with a new perspective for development of rejuvenation agents for synovial joints.

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Identification of the key epigenetic determinants of chondrocyte aging in humans

Project description:This SuperSeries is composed of the SubSeries listed below.

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Transcriptional landscape of aging in humans

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TRIM15 drives chondrocyte senescence and osteoarthritis progression

Project description:Chondrocyte senescence underlies osteoarthritis (OA). However, the pathogenesis of chondrocyte senescence remains largely unclear. Here we report that TRIM15 is a critical regulator in chondrocyte senescence. TIRM15 is highly expressed in chondrocytes of senescent cartilage from human OA patients and aged mice. Using gain- and loss-of-function studies, we further identify that TRIM15 facilitates chondrocyte senescence. Notably, conditional deletion of TRIM15 in chondrocytes severely impairs skeletal growth, partially due to the fact that embryonic chondrocyte senescence is disturbed. Compared with Col2a1-CreERT2/TRIM15flox/flox mice, TRIM15flox/flox mice exhibits accelerated OA phenotype, increased senescence markers and senescence-associated secretory phenotype (SASP) during aging. Mechanistically, TRIM15 binds with YAP and directly mediates K48-linked YAP ubiquitination at K254, which interrupts the interaction between YAP and AMOT, leading to enhanced YAP nuclear translocation. Intra-articular injection of AAV5-Trim15 shRNA decelerates OA progression in mice. Collectively, these findings indicate that targeting TRIM15 reshapes aging cartilage microenvironment and protects against OA.

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