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Upregulation of FOXD1 by YAP alleviates senescence and osteoarthritis

ABSTRACT: Upregulation of FOXD1 by YAP alleviates senescence and osteoarthritis

PROVIDER: PRJNA433339 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6680310_1.fastq.gz	Fastqsanger.gz
	SRR6680310_2.fastq.gz	Fastqsanger.gz
	SRR6680320_1.fastq.gz	Fastqsanger.gz
	SRR6680320_2.fastq.gz	Fastqsanger.gz
	SRR6680291_1.fastq.gz	Fastqsanger.gz

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Upregulation of FOXD1 by YAP alleviates senescence and osteoarthritis

Project description:Cell senescence is a driver of various aging-associated disorders including osteoarthritis. Here, we identified a critical role for Yes-associated protein (YAP), a major effector of Hippo signaling, in maintaining a younger state of human mesenchymal stem cells (MSCs) and ameliorating osteoarthritis in mice. Targeted knockout of YAP in hMSCs resulted in premature cellular senescence. Mechanistically, YAP interacted with TEA domain transcriptional factor (TEAD) to activate forkhead box D1 (FOXD1) expression. YAP deficiency led to the downregulation of FOXD1, a geroprotective protein. In turn, overexpression of YAP or FOXD1 rejuvenated aged hMSCs. Moreover, intra-articular administration of lentiviral vectors encoding YAP or FOXD1 attenuated the development of osteoarthritis in mice. Collectively, our findings reveal YAP-FOXD1, a novel aging-associated regulatory axis, as a potential therapeutic target for gene therapy to alleviate osteoarthritis.

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Up-regulation of FOXD1 by YAP alleviates senescence and osteoarthritis.

Project description:Cellular senescence is a driver of various aging-associated disorders, including osteoarthritis. Here, we identified a critical role for Yes-associated protein (YAP), a major effector of Hippo signaling, in maintaining a younger state of human mesenchymal stem cells (hMSCs) and ameliorating osteoarthritis in mice. Clustered regularly interspaced short palindromic repeat (CRISPR)/CRISPR associated protein 9 nuclease (Cas9)-mediated knockout (KO) of YAP in hMSCs resulted in premature cellular senescence. Mechanistically, YAP cooperated with TEA domain transcriptional factor (TEAD) to activate the expression of forkhead box D1 (FOXD1), a geroprotective protein. YAP deficiency led to the down-regulation of FOXD1. In turn, overexpression of YAP or FOXD1 rejuvenated aged hMSCs. Moreover, intra-articular administration of lentiviral vector encoding YAP or FOXD1 attenuated the development of osteoarthritis in mice. Collectively, our findings reveal YAP-FOXD1, a novel aging-associated regulatory axis, as a potential target for gene therapy to alleviate osteoarthritis.

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