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Ischemic stroke activates hematopoietic bone marrow stem cells.

Gabriel Courties1, Fanny Herisson1, Hendrik B Sager1

  • 1From the Center for Systems Biology, Massachusetts General Hospital and Harvard Medical School, Boston (G.C., H.B.S., T.H., Y.Y., Y.S., P.D., J.S., R.W., F.K.S., M.N.); Stroke and Neurovascular Regulation Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital/Harvard Medical School, Charlestown (F.H., Y.W., M.A.M.); Center for Regenerative Medicine, Massachusetts General Hospital, Boston (N.S., D.T.S.); and Department of Systems Biology, Harvard Medical School, Boston, MA (R.W.).

Circulation Research
|November 2, 2014
PubMed
Summary
This summary is machine-generated.

Ischemic stroke activates hematopoietic stem cells, increasing inflammatory monocyte and neutrophil production. This response is mediated by the sympathetic nervous system and impacts bone marrow hematopoiesis.

Keywords:
bone marrowhematopoietic stem cellsmonocytestroke

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Area of Science:

  • Neuroscience
  • Immunology
  • Hematology

Background:

  • Mechanisms of increased neutrophil and monocyte supply post-stroke are unclear.
  • Stroke-induced immune cell expansion requires understanding hematopoietic stem cell (HSC) regulation.

Purpose of the Study:

  • To investigate if transient middle cerebral artery occlusion (tMCAO) activates HSCs in mice.
  • To elucidate the role of sympathetic tone in stroke-induced hematopoiesis.

Main Methods:

  • In vivo bioluminescence imaging and flow cytometry to assess bone marrow cell cycling.
  • Analysis of hematopoietic transcription factors and progenitor cell populations.
  • Investigating the role of the β3 adrenergic receptor in HSC activation post-stroke.

Main Results:

  • tMCAO significantly increased bone marrow cell cycling and HSC activation.
  • Hematopoiesis showed a myeloid bias, with decreased lymphocyte precursors.
  • Increased sympathetic activity and noradrenaline in bone marrow correlated with HSC activation.
  • Genetic deficiency of the β3 adrenergic receptor blocked HSC cell cycle entry post-tMCAO.

Conclusions:

  • Ischemic stroke activates HSCs through enhanced sympathetic tone.
  • This activation leads to a myeloid-biased hematopoiesis.
  • The bone marrow increases output of inflammatory monocytes and neutrophils post-stroke.