Erratum: Corrigendum: Distinct bone marrow blood vessels differentially regulate haematopoiesis

Itkin, Tomer; Gur-Cohen, Shiri; Spencer, Joel A.; Schajnovitz, Amir; Ramasamy, Saravana K.; Kusumbe, Anjali P.; Ledergor, Guy; Jung, Yookyung; Milo, Idan; Poulos, Michael G.; Kalinkovich, Alexander; Ludin, Aya; Golan, Karin; Khatib, Eman; Kumari, Anju; Shakhar, Guy; Butler, Jason M.; Rafii, Shahin; Adams, Ralf H.; Scadden, David T.; Lin, Charles P.; Lapidot, Tsvee

doi:10.1038/nature19088

Cited by 7 publications

(4 citation statements)

References 1 publication

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“…Despite the presumably high availability of oxygen near blood vessels, we observed low levels of oxidative phosphorylation and high levels of glycolysis within spots immediately adjacent to vascular tissue. These results are consistent with previous data that suggest that endothelial cells, 43 smooth muscle cells, 44 and skeletal stem cells 45 all favor glycolysis as an energy production mechanism to minimize ROS production 43 , 46 and overall gene activation. 47 , 48 Additionally, these results showed elevated levels of transcripts associated with FA metabolism near the cortical bone surface.…”

Section: Discussionsupporting

confidence: 93%

Spatial transcriptomic interrogation of the murine bone marrow signaling landscape

Xiao,

Juan,

Drennon

et al. 2023

Bone Res

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Self-renewal and differentiation of skeletal stem and progenitor cells (SSPCs) are tightly regulated processes, with SSPC dysregulation leading to progressive bone disease. While the application of single-cell RNA sequencing (scRNAseq) to the bone field has led to major advancements in our understanding of SSPC heterogeneity, stem cells are tightly regulated by their neighboring cells which comprise the bone marrow niche. However, unbiased interrogation of these cells at the transcriptional level within their native niche environment has been challenging. Here, we combined spatial transcriptomics and scRNAseq using a predictive modeling pipeline derived from multiple deconvolution packages in adult mouse femurs to provide an endogenous, in vivo context of SSPCs within the niche. This combined approach localized SSPC subtypes to specific regions of the bone and identified cellular components and signaling networks utilized within the niche. Furthermore, the use of spatial transcriptomics allowed us to identify spatially restricted activation of metabolic and major morphogenetic signaling gradients derived from the vasculature and bone surfaces that establish microdomains within the marrow cavity. Overall, we demonstrate, for the first time, the feasibility of applying spatial transcriptomics to fully mineralized tissue and present a combined spatial and single-cell transcriptomic approach to define the cellular components of the stem cell niche, identify cell‒cell communication, and ultimately gain a comprehensive understanding of local and global SSPC regulatory networks within calcified tissue.

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Section: Discussionsupporting

confidence: 93%

Spatial transcriptomic interrogation of the murine bone marrow signaling landscape

Xiao,

Juan,

Drennon

et al. 2023

Bone Res

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“…Arteriolar blood vessels and megakaryocytes comprise HSC niches in the BM (174–176), although they are reported to be spatially and functionally distinct from one another. Sterile, IFNα/β-driven inflammation relocates HSPCs away from quiescence-enforcing arteriolar niches (118), though it is unclear whether this is cause or consequence of changes in HSC cycling.…”

Section: Mechanisms Of Ifnα/β-mediated Hspc Impairmentmentioning

confidence: 99%

Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia

2016

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Aplastic anemia (AA) occurs when the bone marrow fails to support production of all three lineages of blood cells, which are necessary for tissue oxygenation, infection control, and hemostasis. The etiology of acquired AA is elusive in the vast majority of cases but involves exhaustion of hematopoietic stem cells (HSC), which are usually present in the bone marrow in a dormant state, and are responsible for lifelong production of all cells within the hematopoietic system. This destruction is immune mediated and the role of interferons remains incompletely characterized. Interferon gamma (IFNγ) has been associated with AA and type I IFNs (alpha and beta) are well documented to cause bone marrow aplasia during viral infection. In models of infection and inflammation, IFNγ activates HSCs to differentiate and impairs their ability to self-renew, ultimately leading to HSC exhaustion. Recent evidence demonstrating that IFNγ also impacts the HSC microenvironment or niche, raises new questions regarding how IFNγ impairs HSC function in AA. Immune activation can also elicit type I interferons, which may exert effects both distinct from and overlapping with IFNγ on HSCs. IFNα/β increase HSC proliferation in models of sterile inflammation induced by polyinosinic:polycytidylic acid and lead to BM aplasia during viral infection. Moreover, patients being treated with IFNα exhibit cytopenias, in part due to BM suppression. Herein, we review the current understanding of how interferons contribute to the pathogenesis of acquired AA, and we explore additional potential mechanisms by which interferons directly and indirectly impair HSCs. A comprehensive understanding of how interferons impact hematopoiesis is necessary in order to identify novel therapeutic approaches for treating AA patients.

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“…[11][12][13] Definitive HSCs expand and migrate to other tissues throughout the foetus, including the foetal liver, spleen and skin. [14][15][16][17][18] HSCs migrate to the bone marrow (BM) beginning human embryonic week 16, where the microenvironment of extracellular matrix, [19] non-haematopoietic cells, [20,21] chemokines, [22,23] sympathetic signalling [24] and relative hypoxia [25][26][27] enable HSCs to self-renew and divide into the two major lineages of mature blood: lymphoid cells and myeloid cells. [28] Hematopoietic stem cells rapidly expand in response to increased demand for mature blood, through cell-cycle activation dependent on IFN-α, [29] IFN-γ [30] and other cytokines.…”

Section: E X Tr Amedull Ary Haematop Oie S Ismentioning

confidence: 99%

“…Definitive HSCs expand and migrate to other tissues throughout the foetus, including the foetal liver, spleen and skin . HSCs migrate to the bone marrow (BM) beginning human embryonic week 16, where the microenvironment of extracellular matrix, non‐haematopoietic cells, chemokines, sympathetic signalling and relative hypoxia enable HSCs to self‐renew and divide into the two major lineages of mature blood: lymphoid cells and myeloid cells …”

Section: Extramedullary Haematopoiesismentioning

confidence: 99%

Cutaneous extramedullary haematopoiesis: Implications in human disease and treatment

Khalil

Gru

Saavedra

2019

Experimental Dermatology

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The skin and bone marrow are two of the most dynamic organ systems of the human body. While the skin is only transiently involved in haematopoiesis in utero, cutaneous extramedullary haematopoiesis (CEMH) has been appreciated in various neonatal and adult diseases. The mechanism by which CEMH occurs remains poorly understood, but may be associated with the plasticity of blood and skin tissues. Extensive studies have documented expansion and differentiation of haematopoietic lineages from cutaneous tissues and vice versa. This review will discuss CEMH, potential mechanisms and laboratory findings that shed light on the interaction between both tissues. Further, we will discuss the implications of understanding the role of the skin in haematopoiesis, including the potential therapeutic function of manipulating either organ system in the treatment of pathologic processes in the other.

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Erratum: Corrigendum: Distinct bone marrow blood vessels differentially regulate haematopoiesis

Cited by 7 publications

References 1 publication

Spatial transcriptomic interrogation of the murine bone marrow signaling landscape

Spatial transcriptomic interrogation of the murine bone marrow signaling landscape

Hematopoietic Stem Cell Regulation by Type I and II Interferons in the Pathogenesis of Acquired Aplastic Anemia

Cutaneous extramedullary haematopoiesis: Implications in human disease and treatment

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