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Stromal niche inflammation mediated by IL-1 signaling is a targetable driver of hematopoietic aging

ABSTRACT: Stromal niche inflammation mediated by IL-1 signaling is a targetable driver of hematopoietic aging

PROVIDER: PRJNA715585 | ENA |

REPOSITORIES: ENA

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Stromal inflammation is a targetable driver of hematopoietic aging [Microarray analysis]

Project description:Stromal inflammation is a targetable driver of hematopoietic aging [Microarray analysis]

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Stromal inflammation is a targetable driver of hematopoietic aging [droplet-based scRNAseq]

Project description:To investigate global changes in the structure of the bone marrow niche with age, we performed droplet-based scRNAseq (10X Genomics) of unfractionated endosteal and central marrow stromal cells (Ter119-/CD45-). 8,735 cells passed QC, and hematopoietic clusters of cells were excluded based on marker gene expression, leaving 2359 cells distributed across 9 distinct clusters for final presentation.

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Stromal niche inflammation mediated by IL-1 signalling is a targetable driver of haematopoietic ageing.

Project description:Haematopoietic ageing is marked by a loss of regenerative capacity and skewed differentiation from haematopoietic stem cells (HSCs), leading to impaired blood production. Signals from the bone marrow niche tailor blood production, but the contribution of the old niche to haematopoietic ageing remains unclear. Here we characterize the inflammatory milieu that drives both niche and haematopoietic remodelling. We find decreased numbers and functionality of osteoprogenitors at the endosteum and expansion of central marrow LepR+ mesenchymal stromal cells associated with deterioration of the sinusoidal vasculature. Together, they create a degraded and inflamed old bone marrow niche. Niche inflammation in turn drives the chronic activation of emergency myelopoiesis pathways in old HSCs and multipotent progenitors, which promotes myeloid differentiation and hinders haematopoietic regeneration. Moreover, we show how production of interleukin-1β (IL-1β) by the damaged endosteum acts in trans to drive the proinflammatory nature of the central marrow, with damaging consequences for the old blood system. Notably, niche deterioration, HSC dysfunction and defective regeneration can all be ameliorated by blocking IL-1 signalling. Our results demonstrate that targeting IL-1 as a key mediator of niche inflammation is a tractable strategy to improve blood production during ageing.

| S-EPMC7614279 | biostudies-literature

Stromal niche inflammation mediated by IL-1 signaling is a targetable driver of hematopoietic aging

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

2022-11-02 | GSE169162 | GEO

Stromal inflammation is a targetable driver of hematopoietic aging [Microarray analysis]

Project description:We performed integrated analyses of hematopoietic stem and progenitor cells as well as bone marrow stromal cells to better understand the underlying mechanisms of blood aging. To determine how the molecular state of multipotent progenitor (MPP) cells change with age we performed transcriptomic analyses of myeloid-biased MPP3 and lymphoid-biased MPP4 populations from young and old mice.

2022-11-02 | GSE168661 | GEO

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Project description:To investigate the role of IL1 signaling in hematopoietic aging, we performed droplet-based scRNAseq (10X Genomics) of hematopoietic stem and progenitor cells (LK/LSK) and unfractionated endosteal and central marrow stromal cells (Ter119-/CD45-) from young wild type and young and old wild type and IL1R1-/- C57BL/6 mice.

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