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The Journal of Neuroscience, March 29, 2006, 26(13):3491-3495; doi:10.1523/JNEUROSCI.4085-05.2006

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Brief Communications
Involvement of Matrix Metalloproteinase in Neuroblast Cell Migration from the Subventricular Zone after Stroke

Seong-Ryong Lee,^1,3 Hahn-Young Kim,^1,4 Jadwiga Rogowska,⁵ Bing-Qiao Zhao,^1,3 Pradeep Bhide,² Jack M. Parent,⁶ and Eng H. Lo^1,2,7

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

Correspondence should be addressed to Eng H. Lo, Neuroprotection Research Laboratory, Massachusetts General Hospital East 149-2401, Charlestown, MA 02129. Email: Lo{at}helix.mgh.harvard.edu

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.

Key words: neurogenesis; cerebral ischemia; extracellular matrix; stroke recovery; neural precursor; stroke

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Received Sept. 26, 2005; revised Jan. 16, 2006; accepted Jan. 17, 2006.

Correspondence should be addressed to Eng H. Lo, Neuroprotection Research Laboratory, Massachusetts General Hospital East 149-2401, Charlestown, MA 02129. Email: Lo{at}helix.mgh.harvard.edu

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