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Inducible nitric oxide synthase in neutrophils and endothelium contributes to ischemic brain injury in mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Butler, Jason M. Zhou, Ping Anrather, Josef Moore, Jamie M. Racchumi, Gianfranco Garcia-Bonilla, Lidia Iadecola, Costantino
Description	Author Affiliation: Garcia-Bonilla L ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021); Moore JM ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021); Racchumi G ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021); Zhou P ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021); Butler JM ( Department of Genetic Medicine, Weill Cornell Medical College, New York, NY 10021.); Iadecola C ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021); Anrather J ( Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY 10021)
Abstract	NO produced by inducible NO synthase (iNOS) contributes to ischemic brain injury, but the cell types expressing iNOS and mediating tissue damage have not been elucidated. To examine the relative contribution of iNOS in resident brain cells and peripheral leukocytes infiltrating the ischemic brain, we used bone marrow (BM) chimeric mice in which the middle cerebral artery was occluded and infarct volume was determined 3 d later. iNOS(-/-) mice engrafted with iNOS(+/+) BM exhibited larger infarcts (44 ± 2 mm(3); n = 13; mean ± SE) compared with autologous transplanted iNOS(-/-) mice (24 ± 3 mm(3); n = 10; p < 0.01), implicating blood-borne leukocytes in the damage. Furthermore, iNOS(+/+) mice transplanted with iNOS(-/-) BM had large infarcts (39 ± 6 mm(3); n = 13), similar to those of autologous transplanted iNOS(+/+) mice (39 ± 4 mm(3); n = 14), indicating the resident brain cells also play a role. Flow cytometry and cell sorting revealed that iNOS is highly expressed in neutrophils and endothelium but not microglia. Surprisingly, postischemic iNOS expression was enhanced in the endothelium of iNOS(+/+) mice transplanted with iNOS(-/-) BM and in leukocytes of iNOS(-/-) mice with iNOS(+/+) BM, suggesting that endothelial iNOS suppresses iNOS expression in leukocytes and vice versa. To provide independent evidence that neutrophils mediate brain injury, neutrophils were isolated and transferred to mice 24 h after stroke. Consistent with the result in chimeric mice, transfer of iNOS(+/+), but not iNOS(-/-), neutrophils into iNOS(-/-) mice increased infarct volume. The findings establish that iNOS in both neutrophils and endothelium mediates tissue damage and identify these cell types as putative therapeutic targets for stroke injury.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1400918
Journal	The Journal of Immunology
Issue Number	5
Volume Number	193
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2014-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Brain Infarction Immunology Endothelium, Vascular Neutrophils Nitric Oxide Synthase Type Ii Nitric Oxide Stroke Animals Genetics Pathology Endothelial Cells Gene Expression Regulation, Enzymologic Mice Mice, Knockout Time Factors Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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