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Editorial
. 2015 Jan 30;116(3):389-92.
doi: 10.1161/CIRCRESAHA.114.305678.

Waking up the stem cell niche: how hematopoietic stem cells generate inflammatory monocytes after stroke

Dennis Wolf  1 , Klaus Ley  2
Affiliations
Editorial

Waking up the stem cell niche: how hematopoietic stem cells generate inflammatory monocytes after stroke

Dennis Wolf et al. Circ Res. .
No abstract available

Keywords: Editorial; bone marrow; hematopoiesis; monocytes; stem cells; stroke.

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Figures

Figure 1
Figure 1. Proposed mechanism of monocyte release from the bone marrow following stroke
Sympathetic nerve terminals, which end in the bone marrow, secrete noradrenaline after stroke. Noradrenaline binds to β3-adrenergic receptors (ADRB3) expressed on bone marrow stromal cells. In the resting bone marrow, vascular cell adhesion molecule 1 (VCAM-1) binds to the integrin α4β1 (VLA-4) to retain hematopoietic stem cells (HSCs) in the stem cell niche. Additionally, high concentrations of the bone marrow stromal C-X-C motif chemokine 12 (CXCL12) with high affinity to the receptor CXCR-4 expressed on HSCs contribute to their retention. After stroke, expression of VCAM-1 and CXCL12 decreases by a yet undefined mechanism. As a result, HSCs, myeloid progenitor cells, such as GMPs and MDPs, as well as monocytes enter the blood circulation. Moreover, ADRB3 signaling enhances HSC proliferation, increases the myeloid transcription factor PU-1, and generates a myeloid bias with higher numbers of pro-inflammatory Ly6Chigh monocytes. Yet it is unknown, whether stroke-associated monocytosis stroke is protective by improving host defense or detrimental by worsening reperfusion injury and neuronal survival.
See this image and copyright information in PMC

Comment on

  • Ischemic stroke activates hematopoietic bone marrow stem cells.
    Courties G, Herisson F, Sager HB, Heidt T, Ye Y, Wei Y, Sun Y, Severe N, Dutta P, Scharff J, Scadden DT, Weissleder R, Swirski FK, Moskowitz MA, Nahrendorf M. Courties G, et al. Circ Res. 2015 Jan 30;116(3):407-17. doi: 10.1161/CIRCRESAHA.116.305207. Epub 2014 Oct 31. Circ Res. 2015. PMID: 25362208 Free PMC article.

References

    1. Lozano R, Naghavi M, Foreman K, et al. Global and regional mortality from 235 causes of death for 20 age groups in 1990 and 2010: A systematic analysis for the global burden of disease study 2010. Lancet. 2012;380:2095–2128. - PMC - PubMed
    1. Urra X, Arino H, Llull L, Amaro S, Obach V, Cervera A, Chamorro A. The outcome of patients with mild stroke improves after treatment with systemic thrombolysis. PLoS One. 2013;8:e59420. - PMC - PubMed
    1. Courties G, Herisson F, Sager H, et al. Ischemic stroke activates hematopoietic bone marrow stem cells. Circ Res. 2014 - PMC - PubMed
    1. Dutta P, Courties G, Wei Y, et al. Myocardial infarction accelerates atherosclerosis. Nature. 2012;487:325–329. - PMC - PubMed
    1. Heidt T, Sager HB, Courties G, et al. Chronic variable stress activates hematopoietic stem cells. Nat Med. 2014;20:754–758. - PMC - PubMed

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