ArticleCirculation research2015
Ischemic stroke activates hematopoietic bone marrow stem cells.
Article in Circulation research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 papers.
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Who cites it
147 citing papers in PubMed, 232 citations in OpenAlex.
- Bone marrow activation in response to metabolic syndrome and early atherosclerosis.European heart journal · 2022Trial
- A hyperacute immune map of ischaemic stroke patients reveals alterations to circulating innate and adaptive cells.Clinical and experimental immunology · 2021Trial
- CXCL12/CXCR4 signaling governs ischemic neurovascular pathophysiology and repair: a multidimensional contextual analysis.Angiogenesis · 2026Review
- Decoding monocyte signatures in ischemic stroke: A multi-scale transcriptomic approach.Neural regeneration research · 2026Article
- Elevated Plasma T-LAK cell-originated protein kinase Owned the Potential for Predicting Favorable Outcomes in Acute Ischemic Stroke Patients.Cellular and molecular neurobiology · 2026Article
- Neuroinflammation in Ischemic Stroke: Mechanisms, Systemic Interactions, and Therapeutic Targets.Translational stroke research · 2026Review
- Bidirectional brain-heart interactions in health and disease.Nature reviews. Neurology · 2026Review
- Monocyte-derived macrophages and their roles in ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026Review
- Brain heart crosstalk after ischemic stroke toward a unified framework for pathophysiology and precision medicine.Frontiers in molecular neuroscience · 2026Review
- S100A8/A9 inhibition reduces splenic myelopoiesis and improves outcomes after stroke.Frontiers in immunology · 2026Article
- Beyond the usual suspects: rethinking post-stroke immunosuppression.Frontiers in immunology · 2026Review
- Type 2 diabetes Reprograms Bone Marrow Hematopoiesis and Dysregulates Immune Signaling in Response to Stroke.bioRxiv : the preprint server for biology · 2025Article
- Systemic inhibition of soluble TNF significantly changes glial cell populations leading to improved myelin integrity and better functional outcome after experimental stroke.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Article
- Autonomic dysfunction after stroke: an overview of recent clinical evidence and perspectives on therapeutic management.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025Review
- Innate immune memory in macrophage differentiation and cardiovascular diseases.Inflammation and regeneration · 2025Review
- Function of hematopoiesis and bone marrow niche in inflammation and non-hematopoietic diseases.Life medicine · 2025Review
- Neuroimmune Interactions and Their Role in Immune Cell Trafficking in Cardiovascular Diseases and Cancer.International journal of molecular sciences · 2025Review
- Review
- The immunology of stroke and dementia.Immunity · 2025Review
- Stroke in Ghana: A Situational Analysis.Stroke research and treatment · 2025Review
87 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
rationaleThe mechanisms leading to an expanded neutrophil and monocyte supply after stroke are incompletely understood.
objectiveTo test the hypothesis that transient middle cerebral artery occlusion (tMCAO) in mice leads to activation of hematopoietic bone marrow stem cells. METHODS AND
resultsSerial in vivo bioluminescence reporter gene imaging in mice with tMCAO revealed that bone marrow cell cycling peaked 4 days after stroke (P<0.05 versus pre tMCAO). Flow cytometry and cell cycle analysis showed activation of the entire hematopoietic tree, including myeloid progenitors. The cycling fraction of the most upstream hematopoietic stem cells increased from 3.34%±0.19% to 7.32%±0.52% after tMCAO (P<0.05). In vivo microscopy corroborated proliferation of adoptively transferred hematopoietic progenitors in the bone marrow of mice with stroke. The hematopoietic system's myeloid bias was reflected by increased expression of myeloid transcription factors, including PU.1 (P<0.05), and by a decline in lymphocyte precursors. In mice after tMCAO, tyrosine hydroxylase levels in sympathetic fibers and bone marrow noradrenaline levels rose (P<0.05, respectively), associated with a decrease of hematopoietic niche factors that promote stem cell quiescence. In mice with genetic deficiency of the β3 adrenergic receptor, hematopoietic stem cells did not enter the cell cycle in increased numbers after tMCAO (naive control, 3.23±0.22; tMCAO, 3.74±0.33, P=0.51).
conclusionsIschemic stroke activates hematopoietic stem cells via increased sympathetic tone, leading to a myeloid bias of hematopoiesis and higher bone marrow output of inflammatory Ly6C(high) monocytes and neutrophils.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.