상위피인용논문
Abstract
Seong-Ryong Lee1,3, Hahn-Young Kim1,4, Jadwiga Rogowska5, Bing-Qiao Zhao1,3, Pradeep Bhide2, Jack M. Parent6, and Eng H. Lo1,2,7,*
1Neuroprotection Research Laboratory, Departments of Neurology and Radiology, and 2Neuroscience Center, Massachusetts General Hospital, Boston, Massachusetts 02129, 3Department of Pharmacology, Keimyung University, Taegu 700-712, Korea, 4Department of Neurology, Konkuk University, Seoul 143-701, Korea, 5Department of Psychiatry, McLean Hospital, Belmont, Massachusetts 02478, 6Department of Neurology, University of Michigan Medical School, Ann Arbor, Michigan 48109, and 7Program in Neuroscience, Harvard Medical School, Boston, Massachusetts 02115
*Corresponding author
Abstract
After brain injury, neuroblast cells from the subventricular zone (SVZ) expand and migrate toward damaged tissue. The mechanisms that mediate these neurogenic and migratory responses remain to be fully dissected. Here, we show that bromodeoxyuridine-labeled and doublecortin-positive cells from the SVZ colocalize with the extracellular protease matrix metalloproteinase-9 (MMP-9) during the 2 week recovery period after transient focal cerebral ischemia in mice. Treatment with the broad spectrum MMP inhibitor GM6001 significantly decreases the migration of doublecortin-positive cells that extend from the SVZ into the striatum. These data suggest that MMPs are involved in endogenous mechanisms of neurogenic migration as the brain seeks to heal itself after injury.
neurogenesis, cerebral ischemia, extracellular matrix, stroke recovery, neural precursor, stroke
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