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Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

ABSTRACT: Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

PROVIDER: PRJNA1067582 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27679282.fastq.gz	Fastqsanger.gz
	SRR27679283.fastq.gz	Fastqsanger.gz

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Cellular and functional characterization of aging-independent senescent-like cells that modulate tissue repair

Project description:Cells expressing features of cellular senescence, including upregulation of p21 and p16, appear transiently following tissue injury, yet the properties of these cells or how they contrast with age-induced senescent cells remains unclear. Using skeletal fracture as a model of acute injury, we identified rapidly-appearing senescent-like cells, marked by p21 expression, that negatively affected fracture healing. p21+ callus cells, which consisted predominantly of neutrophils and osteochondroprogenitors, existed as transient cells specific to injury and expressed high levels of senescence-associated factors known to impair bone formation and induce paracrine senescence. Targeted genetic clearance of p21+ cells suppressed senescence-associated signatures within the fracture callus and accelerated fracture healing. By contrast, p21+ cell clearance did not alter bone loss due to aging; conversely, p16+ cell clearance, known to alleviate skeletal aging, did not affect fracture healing. Together, our findings establish contextual roles of senescent/senescent-like cells that may be leveraged for therapeutic opportunities.

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Accumulating DNA damage and insufficient DNA repair in senescent cells underlie persistent DNA damage signaling

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