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Recruitment of bone marrow stromal cells in the cerebral microvasculature after focal ischemia‐reperfusion is mediated by selectins
Author(s) -
Yilmaz Gokhan,
Vital Shantel,
Stokes Karen Y.,
Granger D. Neil
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a1275-a
Subject(s) - stromal cell , selectin , bone marrow , medicine , stroke (engine) , endothelium , ischemia , intravital microscopy , pathology , reperfusion injury , mesenchymal stem cell , e selectin , brain ischemia , cell adhesion molecule , adhesion , cell adhesion , immunology , chemistry , microcirculation , mechanical engineering , organic chemistry , engineering
The therapeutic potential of bone marrow stromal cells (BMSC) has been demonstrated in different models of stroke. While it is well known that BMSC migrate and home to the site of brain injury, the mechanism underlying this cell recruitment is not known. We hypothesize that after stroke, cerebrovascular endothelium expresses adhesion molecules that allow BMSC to recognize and home to the injury site. Stroke was induced in C57BL/6 mice by middle cerebral artery occlusion (MCAo) for 1 h, followed by 24 h reperfusion (MCAo/R). BMSC from H‐2Kb‐tsA58 mice were fluorescently labeled and administered (24 h after stroke) i.v. with or without an E‐ or P‐selectin blocking antibody. BMSC were observed in cortical vessels using intravital microscopy. Significant adhesion (76±5 cells/mm 2 ) of BMSC was observed in venules after MCAo/R, while a low number of adherent BMSC was detected in sham mice (16±4 cells/mm 2 ). E‐ and P‐selectin antibodies blocked the adhesion of BMSC in cerebral venules after stroke (36 ±4 & 10±3 cells/mm 2 respectively). These findings indicate that cerebral endothelium assume a pro‐adhesive phenotype following MCAO/R that favors the recruitment of BMSC into the infarct area. This adhesive interface between the blood and endothelial cell surface represents an important therapeutic target for enhancement of stem cell delivery to sites of ischemic infarction following stroke. (HL26441)