This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zhao, B.-Q. Articles by Lo, E. H. Search for Related Content PubMed PubMed Citation Articles by Zhao, B.-Q. Articles by Lo, E. H. Pubmed/NCBI databases Substance via MeSH Medline Plus Health Information Stroke Traumatic Brain Injury Related Collections Animal models of human disease Acute Cerebral Hemorrhage Acute Cerebral Infarction

(Stroke. 2007;38:748.)
© 2007 American Heart Association, Inc.

Intracerebral Hemorrhage: Introduction

Neurovascular Proteases in Brain Injury, Hemorrhage and Remodeling After Stroke

Bing-Qiao Zhao, MD; Emiri Tejima, MD Eng H. Lo, PhD

From the Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital, and Program in Neuroscience, Harvard Medical School, Boston, Mass.

Correspondence to Eng H. Lo, Neuroprotection Research Laboratory, Massachusetts General Hospital, East 149-2401, Charlestown, MA 02129. E-mail Lo{at}helix.mgh.harvard.edu

Abstract

Matrix metalloproteinases (MMPs) mediate tissue injury during acute stroke. Clinical data show that elevated MMPs in plasma of stroke patients may correlate with outcomes, suggesting its use as a biomarker. MMP-9 signal has also been detected in clinical stroke brain tissue samples. Because tissue plasminogen activator can upregulate MMPs via lipoprotein receptor signaling, these neurovascular proteolytic events may underlie some of the complications of edema and hemorrhage that plague thrombolytic therapy. However, in contrast to its deleterious actions in acute stroke, MMPs and other neurovascular proteases may play beneficial roles during stroke recovery. MMPs are increased in the subventricular zone weeks after focal stroke, and inhibition of MMPs suppress neurogenic migration from subventricular zone into damaged tissue. In peri-infarct cortex, MMPs may mediate neurovascular remodeling. Delayed inhibition of MMPs decrease markers of remodeling, and these phenomena may be related to reductions in bioavailable growth factors. Acute versus chronic protease profiles within the neurovascular unit are likely to underlie critical responses to stroke, therapy, and recovery.

Key Words: matrix proteins • neuroregeneration • pathology ischemia

This article has been cited by other articles:

				B. W. McColl, N. J. Rothwell, and S. M. Allan Systemic Inflammation Alters the Kinetics of Cerebrovascular Tight Junction Disruption after Experimental Stroke in Mice J. Neurosci., September 17, 2008; 28(38): 9451 - 9462. [Abstract] [Full Text] [PDF]

				E. E. Benarroch Tissue plasminogen activator: Beyond thrombolysis Neurology, August 21, 2007; 69(8): 799 - 802. [Full Text] [PDF]