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ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [RNA-seq]

ABSTRACT: ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [RNA-seq]

PROVIDER: PRJNA838486 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19217353_1.fastq.gz	Fastqsanger.gz
	SRR19217353_2.fastq.gz	Fastqsanger.gz
	SRR19217354_1.fastq.gz	Fastqsanger.gz
	SRR19217354_2.fastq.gz	Fastqsanger.gz
	SRR19217355_1.fastq.gz	Fastqsanger.gz

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ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [RNA-seq]

Project description:Defining mechanism(s) that maintain tissue stem quiescence is important for improving tissue regeneration, cell therapies, aging, and cancer. We report here that genetic ablation of Id2 in adult hematopoietic stem cells (HSCs) promotes increased HSC activation and differentiation, which results in HSC exhaustion and bone marrow failure over time. Id2Δ/Δ HSCs show increased HSC cycling, reactive oxygen species (ROS) production, mitochondrial activation, and DNA damage supporting the conclusion that Id2Δ/Δ HSCs are less quiescent. Mechanistically, HIF-1α expression is decreased in Id2Δ/Δ HSCs, and stabilization of HIF-1α in Id2Δ/Δ HSCs restores HSC quiescence and rescues HSC exhaustion. ID2 promotes HIF-1α expression by binding to the Von Hippel-Lindau (VHL) protein and interfering with proteasomal degradation of HIF-1α. HIF-1α promotes Id2 expression and enforces a positive feedback loop between ID2 and HIF-1α to maintain HSC quiescence. Thus, sustained ID2 expression could protect HSCs during stress, and improve HSC expansion for gene editing and cell therapies.

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ID2 and HIF-1α collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [scRNA-seq]

Project description:Defining mechanism(s) that maintain tissue stem quiescence is important for improving tissue regeneration, cell therapies, aging, and cancer. We report here that genetic ablation of Id2 in adult hematopoietic stem cells (HSCs) promotes increased HSC activation and differentiation, which results in HSC exhaustion and bone marrow failure over time. Id2Δ/Δ HSCs show increased cycling, reactive oxygen species (ROS) production, mitochondrial activation, ATP production, and DNA damage compared to Id2+/+ HSCs, supporting the conclusion that Id2Δ/Δ HSCs are less quiescent. Mechanistically, HIF-1α expression is decreased in Id2Δ/Δ HSCs, and stabilization of HIF-1α in Id2Δ/Δ HSCs restores HSC quiescence and rescues HSC exhaustion. ID2 promotes HIF-1α expression by binding to the Von Hippel-Lindau (VHL) protein and interfering with proteasomal degradation of HIF-1α. HIF-1α promotes Id2 expression and enforces a positive feedback loop between ID2 and HIF-1α to maintain HSC quiescence. Thus, sustained ID2 expression could protect HSCs during stress, and improve HSC expansion for gene editing and cell therapies.

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ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion

Project description:ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion

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ID2 and HIF-1α collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [scRNA-seq]

Project description:ID2 and HIF-1α collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion [scRNA-seq]

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ID2 and HIF-1α collaborate to protect quiescent hematopoietic stem cells from activation, differentiation, and exhaustion.

Project description:Defining mechanism(s) that maintain tissue stem quiescence is important for improving tissue regeneration, cell therapies, aging, and cancer. We report here that genetic ablation of Id2 in adult hematopoietic stem cells (HSCs) promotes increased HSC activation and differentiation, which results in HSC exhaustion and bone marrow failure over time. Id2Δ/Δ HSCs showed increased cycling, ROS production, mitochondrial activation, ATP production, and DNA damage compared with Id2+/+ HSCs, supporting the conclusion that Id2Δ/Δ HSCs are less quiescent. Mechanistically, HIF-1α expression was decreased in Id2Δ/Δ HSCs, and stabilization of HIF-1α in Id2Δ/Δ HSCs restored HSC quiescence and rescued HSC exhaustion. Inhibitor of DNA binding 2 (ID2) promoted HIF-1α expression by binding to the von Hippel-Lindau (VHL) protein and interfering with proteasomal degradation of HIF-1α. HIF-1α promoted Id2 expression and enforced a positive feedback loop between ID2 and HIF-1α to maintain HSC quiescence. Thus, sustained ID2 expression could protect HSCs during stress and improve HSC expansion for gene editing and cell therapies.

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ID2 and HIF-1α Collaborate to Protect Quiescent Hematopoietic Stem Cells from Activation, Differentiation and Exhaustion

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