Leukocyte_derived matrix metalloproteinase_9 mediates blood_brain barrier breakdown and is.pdf
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Leukocyte_derived matrix metalloproteinase_9 mediates blood_brain barrier breakdown and is
Leukocyte-derived matrix metalloproteinase-9 mediates blood-brain barrier
breakdown and is proinflammatory after transient focal cerebral ischemia
Jeffrey M. Gidday,1,2,4 Yvan G. Gasche,5,7 Jean-C. Copin,5,7 Aarti R. Shah,1
Ronald S. Perez,1 Steven D. Shapiro,6 Pak H. Chan,7 and T. S. Park1,3,4
Departments of 1Neurosurgery, 2Cell Biology and Physiology, and 3Anatomy and Neurobiology, Washington
University School of Medicine, and 4St. Louis Children’s Hospital, St. Louis, Missouri; 5Departments of
Anesthesiology, Pharmacology, Surgical Critical Care and Internal Medicine, and Neuroscience, Geneva University,
Geneva, Switzerland; 6Pulmonary and Critical Care Medicine, Brigham and Women’s Hospital and Harvard
Medical School, Boston, Massachusetts; and 7Department of Neurosurgery and Department of Neurology and
Neurological Sciences and Program in Neuroscience, Stanford University School of Medicine, Stanford, California
Submitted 16 December 2004; accepted in final form 4 March 2005
Gidday, Jeffrey M., Yvan G. Gasche, Jean-C. Copin, Aarti
R. Shah, Ronald S. Perez, Steven D. Shapiro, Pak H. Chan, and
T. S. Park. Leukocyte-derived matrix metalloproteinase-9 medi-
ates blood-brain barrier breakdown and is proinflammatory after
transient focal cerebral ischemia. Am J Physiol Heart Circ Physiol
289: H558 –H568, 2005. First published March 11, 2005;
doi:10.1152/ajpheart.01275.2004.—Results of recent studies re-
veal vascular and neuroprotective effects of matrix metalloprotein-
ase-9 (MMP-9) inhibition and MMP-9 gene deletion in experimen-
tal stroke. However, the cellular source of MMP-9 produced in the
ischemic brain and the mechanistic basis of MMP-9-mediated
brain injury require elucidation. In the present study, we used
MMP-9/ mice and chimeric knockouts lacking either MMP-9 in
leukocytes or in resident brain cells to test the hypothesis that
MMP-9 released from leukocytes recruited to the brain during
postischemic reperfusion contributes to this injury phenotype. We
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