Journal
JOURNAL OF NEUROTRAUMA
Volume 32, Issue 20, Pages 1553-1559Publisher
MARY ANN LIEBERT, INC
DOI: 10.1089/neu.2014.3764
Keywords
adult brain injury; extracellular matrix; microdialysis
Funding
- National Institute for Health Research (NIHR) Academic Clinical Fellowship
- Royal College of Surgeons/Philip King Research Fellowship
- Beverley and Raymond Sackler Fellowship
- joint Medical Research Council/Royal College of Surgeons of England Clinical Research Training Fellowship
- NIHR Biomedical Research Center, Cambridge
- Traumatic Brain Injury NIHR Health Technology Cooperative
- NIHR Senior Investigator Award
- Cambridge NIHR BRC
- NIHR Research Professorship
- Medical Research Council [G1002277] Funding Source: researchfish
- National Institute for Health Research [NIHR-RP-R3-12-013, NF-SI-0512-10090] Funding Source: researchfish
- MRC [G1002277] Funding Source: UKRI
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Matrix metalloproteinases (MMPs) are extracellular enzymes that have been implicated in the pathophysiology of blood-brain barrier (BBB) breakdown, contusion expansion, and vasogenic edema after traumatic brain injury (TBI). Specifically, in focal injury models, increased MMP-9 expression has been observed in pericontusional brain, and MMP-9 inhibitors reduce brain swelling and final lesion volume. The aim of this study was to examine whether there is a similarly localized increase of MMP concentrations in patients with contusional TBI. Paired microdialysis catheters were inserted into 12 patients with contusional TBI (with or without associated mass lesion) targeting pericontusional and radiologically normal brain defined on admission computed tomography scan. Microdialysate was pooled every 8h and analyzed for MMP-1, -2, -7, -9, and -10 using a multiplex immunoassay. Concentrations of MMP-1, -2, and -10 were similar at both monitoring sites and did not show discernible temporal trends. Overall, there was a gradual increase in MMP-7 concentrations in both normal and injured brain over the monitoring period, although this was not consistent in every patient. MMP-9 concentrations were elevated in pericontusional, compared to normal, brain, with the maximal difference at the earliest monitoring times (i.e., <24h postinjury). Repeated-measures analysis of variance showed that MMP-9 concentrations were significantly higher in pericontusional brain (p=0.03) and within the first 72h of injury, compared with later in the monitoring period (p=0.04). No significant differences were found for the other MMPs assayed. MMP-9 concentrations are increased in pericontusional brain early post-TBI and may represent a potential therapeutic target to reduce hemorrhagic progression and vasogenic edema.
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