Inflammation and Aging of Hematopoietic Stem Cells in Their Niche

Yang, Daozheng; Haan, Gerald de

doi:10.3390/cells10081849

Cited by 31 publications

(16 citation statements)

References 102 publications

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“…On the one hand, transient inflammation promotes the proliferation of precursor/stem cells [ 68 , 72 ]. On the other hand, it also contributes to the aging of these cells, such as proinflammatory cytokines IL-1β, TNF-α and IL-6 in mediating aging of hematopoietic stem cells (HSCs) if without resolution [ 73 ]. In addition, different types of stem cells produce distinct characterizations and responses to inflammatory stimulation [ 74 ].…”

Section: Crosstalk Between Inflammation and Blastemal Cells Or Immature Somatic Cellsmentioning

confidence: 99%

Self-Control of Inflammation during Tail Regeneration of Lizards

Song

Wang

2021

JDB

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Lizards can spontaneously regenerate their lost tail without evoking excessive inflammation at the damaged site. In contrast, tissue/organ injury of its mammalian counterparts results in wound healing with a formation of a fibrotic scar due to uncontrolled activation of inflammatory responses. Unveiling the mechanism of self-limited inflammation occurring in the regeneration of a lizard tail will provide clues for a therapeutic alternative to tissue injury. The present review provides an overview of aspects of rapid wound healing and roles of antibacterial peptides, effects of leukocytes on the tail regeneration, self-blocking of the inflammatory activation in leukocytes, as well as inflammatory resistance of blastemal cells or immature somatic cells during lizard tail regeneration. These mechanistic insights of self-control of inflammation during lizard tail regeneration may lead in the future to the development of therapeutic strategies to fight injury-induced inflammation.

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Section: Crosstalk Between Inflammation and Blastemal Cells Or Immature Somatic Cellsmentioning

confidence: 99%

Self-Control of Inflammation during Tail Regeneration of Lizards

Song

Wang

2021

JDB

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“…HSC are sustained by specific niche cells of the bone marrow microenvironment, namely, by endothelial cells present in the microvasculature [ 45 ]. Evidence is emerging, however, that the nature of the supporting niche changes with age and/or under inflammatory states, although the identity of the cells supporting the HSC under these conditions has not been clarified as yet [ 46 , 47 ]. In addition, MPN is associated with profound differences in the composition of the cells of the microenvironment.…”

Section: Resultsmentioning

confidence: 99%

“…Numerous studies are currently analyzing the changes occurring at the level of HSC with aging under the assumption that these changes may predispose to the development of myeloproliferative disorders and possibly to leukemia. Aging affects the HSC directly, by inducing epigenetic changes, and indirectly, by altering the supportive role of the microenvironment [ 46 , 47 , 71 ]. These effects are supposed to be mediated by proinflammatory cytokines produced by the organism in response to environmental insults [ 72 ].…”

Section: Discussionmentioning

confidence: 99%

“…The last few years have seen a great increase in our understanding of the niches supporting hematopoiesis in the bone marrow. The HSC niches in the murine bone marrow are defined based on their anatomical location (in the diaphysis or in the epiphysis of the femur), the type of blood vessels (sinusoids, arterioles of transition zone vessels) they contain, and the proximity with the endosteal zone [ 45 , 46 , 47 ]. Based on their anatomical site, at least two different types of HSC have been recognized: the central niche, which contains sinusoids and arterioles and hosts the majority (>90%) of the HSC, and the endosteal niche, in close proximity to the bone surface, which hosts the rest of the HSC.…”

Section: Discussionmentioning

confidence: 99%

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Resident Self-Tissue of Proinflammatory Cytokines Rather Than Their Systemic Levels Correlates with Development of Myelofibrosis in Gata1low Mice

et al. 2022

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Serum levels of inflammatory cytokines are currently investigated as prognosis markers in myelofibrosis, the most severe Philadelphia-negative myeloproliferative neoplasm. We tested this hypothesis in the Gata1low model of myelofibrosis. Gata1low mice, and age-matched wild-type littermates, were analyzed before and after disease onset. We assessed cytokine serum levels by Luminex-bead-assay and ELISA, frequency and cytokine content of stromal cells by flow cytometry, and immunohistochemistry and bone marrow (BM) localization of GFP-tagged hematopoietic stem cells (HSC) by confocal microscopy. Differences in serum levels of 32 inflammatory-cytokines between prefibrotic and fibrotic Gata1low mice and their wild-type littermates were modest. However, BM from fibrotic Gata1low mice contained higher levels of lipocalin-2, CXCL1, and TGF-β1 than wild-type BM. Although frequencies of endothelial cells, mesenchymal cells, osteoblasts, and megakaryocytes were higher than normal in Gata1low BM, the cells which expressed these cytokines the most were malignant megakaryocytes. This increased bioavailability of proinflammatory cytokines was associated with altered HSC localization: Gata1low HSC were localized in the femur diaphysis in areas surrounded by microvessels, neo-bones, and megakaryocytes, while wild-type HSC were localized in the femur epiphysis around adipocytes. In conclusion, bioavailability of inflammatory cytokines in BM, rather than blood levels, possibly by reshaping the HSC niche, correlates with myelofibrosis in Gata1low mice.

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“…During aging, tissue-specific alterations in the niche synergize with stem cell-intrinsic changes to contribute to the development of age-associated traits 17,[70][71][72] . Aging has been proposed to drive a pro-inflammatory microenvironment that perturbs adult stem cell behavior in several tissues, including that of neural, skeletal and hematopoietic stem cells [73][74][75][76] . Interestingly, the nature of these signals is highly tissue-dependent and include infiltration of immune cells into the stem cell niche 73 , or a transcriptional switch of the stem cells that create a pro-inflammatory environment that negatively feeds back to their own fitness 74 .…”

Section: Discussionmentioning

confidence: 99%

Local IL-17 orchestrates skin aging

Solá

Mereu

Bonjoch

et al. 2022

Preprint

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Skin aging is characterized by structural and functional changes that lead to slower wound healing and higher rate of infections, which contribute to age-associated frailty. This likely depends on synergy between alterations in the local microenvironment and stem cell–intrinsic changes, underscored by pro-inflammatory microenvironments that drive pleotropic changes. To date, little is known about the precise nature and origin of the proposed age-associated inflammatory cues, or how they affect different tissue resident cell types. Based on deep single-cell RNA-sequencing of the entire dermal compartment, we now provide a comprehensive understanding of the age-associated changes in all skin cell types. We show a previously unreported skew towards an IL-17–expressing phenotype of Th cells, γδ T cells and innate lymphoid cells in aged skin. Aberrant IL-17 signaling is common to many autoimmune (e.g., rheumatoid arthritis and psoriasis) and chronic inflammatory diseases. Importantly, in vivo blockade of IL-17–triggered signaling during the aging process reduces the pro-inflammatory state by affecting immune and non-immune skin cells of both dermis and epidermis. Strikingly, IL-17 neutralization significantly delays the appearance of age-related traits, such as decreased epidermal thickness, increased cornified layer thickness and ameliorated hair follicle stem cell activation and hair shaft regeneration. Our results indicate that the aged skin shows chronic and persistent signs of inflammation, and that age-associated increased IL-17 signaling could be targeted as a strategy to prevent age-associated skin ailments in elderly.

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Inflammation and Aging of Hematopoietic Stem Cells in Their Niche

Cited by 31 publications

References 102 publications

Self-Control of Inflammation during Tail Regeneration of Lizards

Self-Control of Inflammation during Tail Regeneration of Lizards

Resident Self-Tissue of Proinflammatory Cytokines Rather Than Their Systemic Levels Correlates with Development of Myelofibrosis in Gata1low Mice

Local IL-17 orchestrates skin aging

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