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Temporal multimodal single-cell profiling of native hematopoiesis illuminates altered differentiation trajectories with age

ABSTRACT: Temporal multimodal single-cell profiling of native hematopoiesis illuminates altered differentiation trajectories with age

PROVIDER: PRJNA733218 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14670369.fastq.gz	Fastqsanger.gz
	SRR14670370.fastq.gz	Fastqsanger.gz
	SRR14670371.fastq.gz	Fastqsanger.gz
	SRR14670372.fastq.gz	Fastqsanger.gz
	SRR14670373.fastq.gz	Fastqsanger.gz

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Temporal multimodal single-cell profiling of native hematopoiesis illuminates altered differentiation trajectories with age

Project description:Aging impacts negatively on hematopoiesis, with consequences for immunity and acquired blood cell disorders. While impairments in hematopoietic stem cell (HSC) function contribute to this, the in vivo dynamics of such changes remain obscure. Here, we integrate extensive longitudinal functional assessments of HSC-specific lineage tracing with single-cell transcriptome and epitope profiling. In contrast to recent suggestions from single-cell RNA sequencing alone, our data favor a defined structure of HSC/progenitor differentiation that deviates substantially from HSC-derived hematopoiesis following transplantation. Native age-dependent attrition in HSC differentiation manifests as a drastically reduced lymphoid output via an early lymphoid-primed progenitor (MPP Ly-I). While in vitro activation fails to rescue lymphoid differentiation from most aged HSCs, robust lymphopoiesis can be achieved by culturing elevated numbers of candidate HSCs. Therefore, our data position rare chronologically aged HSC clones, fully competent at producing lymphoid offspring, as prime target for approaches aimed to improve lymphopoiesis in the elderly.

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HSCs contribute actively to native multilineage hematopoiesis but with reduced differentiation capacity upon aging

Project description:A hallmark of adult hematopoiesis is the continuous replacement of blood cells with limited lifespans. While active hematopoietic stem cell (HSC) contribution to multilineage hematopoiesis is the foundation of clinical HSC transplantation, recent reports have questioned the physiological contribution of HSCs to normal/steady-state adult hematopoiesis. Here, we use inducible lineage tracing from genetically marked adult HSCs and reveal robust HSC-derived multilineage hematopoiesis. This commences via defined progenitor cells, but varies substantially in between different hematopoietic lineages. By contrast, adult HSC contribution to hematopoietic cells with proposed fetal origins is neglible. Finally, we establish that the HSC contribution to multilineage hematopoiesis declines with increasing age. Therefore, while HSCs are active contributors to native adult hematopoiesis, it appears that the numerical increase of HSCs is a physiologically relevant compensatory mechanism to account for their reduced differentiation capacity with age

2018-12-18 | GSE122473 | GEO

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