Reduced Matrix Metalloproteinase-9 Activity and Cell Death After Global Ischemia in the Brain Preconditioned with Hyperbaric Oxygen

2009 ◽  
pp. 47-49 ◽  
Author(s):  
Robert P. Ostrowski ◽  
Vikram Jadhav ◽  
Wanqiu Chen ◽  
John H. Zhang
Keyword(s):  
Cell Death ◽  
Matrix Metalloproteinase ◽  
Hyperbaric Oxygen ◽  
Matrix Metalloproteinase 9 ◽  
Global Ischemia ◽  
The Brain ◽  
Metalloproteinase 9

Matrix metalloproteinase 9 regulates cell death following pilocarpine-induced seizures in the developing brain

2012 ◽  
Vol 48 (3) ◽  
pp. 339-347 ◽  
Author(s):  
Yvonne Hoehna ◽  
Ortrud Uckermann ◽  
Hella Luksch ◽  
Vanya Stefovska ◽  
Jenny Marzahn ◽  
...  
Keyword(s):  
Cell Death ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Developing Brain ◽  
Metalloproteinase 9

Increased matrix-metalloproteinase-2 and matrix-metalloproteinase-9 expression in the brain of dystrophic mdx mouse

Neuroscience ◽  
2006 ◽  
Vol 140 (3) ◽  
pp. 835-848 ◽  
Author(s):  
B. Nico ◽  
P. Corsi ◽  
R. Ria ◽  
E. Crivellato ◽  
A. Vacca ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 9 ◽  
Matrix Metalloproteinase 2 ◽  
Mdx Mouse ◽  
The Brain ◽  
Metalloproteinase 9

Hyperbaric oxygen therapy accelerates wound healing in diabetic mice by decreasing active matrix metalloproteinase‐9

2019 ◽  
Vol 28 (2) ◽  
pp. 194-201 ◽  
Author(s):  
Trung T. Nguyen ◽  
Jeffrey I. Jones ◽  
William R. Wolter ◽  
Rocio L. Pérez ◽  
Valerie A. Schroeder ◽  
...  
Keyword(s):  
Wound Healing ◽  
Matrix Metalloproteinase ◽  
Hyperbaric Oxygen ◽  
Hyperbaric Oxygen Therapy ◽  
Oxygen Therapy ◽  
Matrix Metalloproteinase 9 ◽  
Diabetic Mice ◽  
Active Matrix ◽  
Metalloproteinase 9

Leukocyte-derived matrix metalloproteinase-9 mediates blood-brain barrier breakdown and is proinflammatory after transient focal cerebral ischemia

2005 ◽  
Vol 289 (2) ◽  
pp. H558-H568 ◽  
Author(s):  
Jeffrey M. Gidday ◽  
Yvan G. Gasche ◽  
Jean-C. Copin ◽  
Aarti R. Shah ◽  
Ronald S. Perez ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Blood Brain Barrier ◽  
Matrix Metalloproteinase 9 ◽  
Leukocyte Recruitment ◽  
Brain Barrier ◽  
Ischemic Brain ◽  
Blood Brain ◽  
Cellular Source ◽  
The Brain ◽  
Metalloproteinase 9

Results of recent studies reveal vascular and neuroprotective effects of matrix metalloproteinase-9 (MMP-9) inhibition and MMP-9 gene deletion in experimental 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 also tested the hypothesis that MMP-9 promotes leukocyte recruitment to the ischemic brain and thus is proinflammatory. The extent of blood-brain barrier (BBB) breakdown, the neurological deficit, and the volume of infarction resulting from transient focal stroke were abrogated to a similar extent in MMP-9−/−mice and in chimeras lacking leukocytic MMP-9 but not in chimeras with MMP-9-containing leukocytes. Zymography and Western blot analysis from these chimeras confirmed that the elevated MMP-9 expression in the brain at 24 h of reperfusion is derived largely from leukocytes. MMP-9−/−mice exhibited a reduction in leukocyte-endothelial adherence and a reduction in the number of neutrophils plugging capillaries and infiltrating the ischemic brain during reperfusion; microvessel immunopositivity for collagen IV was also preserved in these animals. These latter results document proinflammatory actions of MMP-9 in the ischemic brain. Overall, our findings implicate leukocytes, most likely neutrophils, as a key cellular source of MMP-9, which, in turn, promotes leukocyte recruitment, causes BBB breakdown secondary to microvascular basal lamina proteolysis, and ultimately contributes to neuronal injury after transient focal stroke.

scholarly journals Matrix Metalloproteinase 9 Facilitates West Nile Virus Entry into the Brain

2008 ◽  
Vol 82 (18) ◽  
pp. 8978-8985 ◽  
Author(s):  
Penghua Wang ◽  
Jianfeng Dai ◽  
Fengwei Bai ◽  
Kok-Fai Kong ◽  
Susan J. Wong ◽  
...  
Keyword(s):  
West Nile Virus ◽  
Matrix Metalloproteinase ◽  
Blood Brain Barrier ◽  
Matrix Metalloproteinase 9 ◽  
Brain Barrier ◽  
West Nile ◽  
Blood Brain ◽  
Mmp9 Expression ◽  
The Brain ◽  
Metalloproteinase 9

ABSTRACT West Nile virus (WNV) is the most-common cause of mosquito-borne encephalitis in the United States. Invasion of the brain by WNV is influenced by viral and host factors, and the molecular mechanism underlying disruption of the blood-brain barrier is likely multifactorial. Here we show that matrix metalloproteinase 9 (MMP9) is involved in WNV entry into the brain by enhancing blood-brain barrier permeability. Murine MMP9 expression was induced in the circulation shortly after WNV infection, and the protein levels remained high even when viremia subsided. In the murine brain, MMP9 expression and its enzymatic activity were upregulated and MMP9 was shown to partly localize to the blood vessels. Interestingly, we also found that cerebrospinal fluid from patients suffering from WNV contained increased MMP9 levels. The peripheral viremia and expression of host cytokines were not altered in MMP9 −/− mice; however, these animals were protected from lethal WNV challenge. The resistance of MMP9 −/− mice to WNV infection correlated with an intact blood-brain barrier since immunoglobulin G, Evans blue leakage into brain, and type IV collagen degradation were markedly reduced in the MMP9 −/− mice compared with their levels in controls. Consistent with this, the brain viral loads, selected inflammatory cytokines, and leukocyte infiltrates were significantly reduced in the MMP9 −/− mice compared to their levels in wild-type mice. These data suggest that MMP9 plays a role in mediating WNV entry into the central nervous system and that strategies to interrupt this process may influence the course of West Nile encephalitis.

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