Literature DB >> 17673717

Matrix metalloproteinase-9 inhibition attenuates vascular endothelial growth factor-induced intracerebral hemorrhage.

Chanhung Z Lee1, Zheng Xue, Yiqian Zhu, Guo-Yuan Yang, William L Young.   

Abstract

BACKGROUND AND
PURPOSE: Human brain arteriovenous malformation tissue displays increased levels of vascular endothelial growth factor (VEGF) as well as matrix metalloproteinase (MMP)-9, a tissue protease associated with various intracerebral hemorrhage (ICH). We hypothesized that increased MMP-9 was associated with ICH induced by vascular endothelial growth factor hyperstimulation and that this effect could be attenuated by nonspecific MMP inhibition.
METHODS: We used a mouse model with adenoviral vector-mediated vascular endothelial growth factor transduction in the brain. The association of MMP-9 expression and the brain tissue hemoglobin levels, an index of ICH, after stereotactic injection of adenoviral vector-mediated vascular endothelial growth factor into caudate putamen was assessed. A dose-response study with adenoviral vector-mediated vascular endothelial growth factor and a time course study at both 24 and 48 hours postinjection were performed. Effects of minocycline, a nonspecific MMP inhibitor, and pyrrolidine dithiocarbamate, an upstream regulator of MMPs, on MMP-9 activity and thereby the degree of ICH were also tested.
RESULTS: Adenoviral vector-mediated vascular endothelial growth factor at the higher dose and at 48 hours induced MMP-9 levels 6-fold (n=6, P=0.02) and increased brain tissue hemoglobin (43.4+/-11.5 versus 30.3+/-4.1 mug/mg, n=6, P=0.003) compared with the adenoviral vector control. Immnunostaining was positive for MMP-9 around the cerebral vessels and the hemorrhagic areas. Minocycline and pyrrolidine dithiocarbamate administration suppressed vascular endothelial growth factor-induced MMP-9 activity (n=6, P=0.003 and P=0.01, respectively) and the associated increases in hemoglobin levels (n=5-6, P=0.001 and P=0.02, respectively).
CONCLUSIONS: Vascular endothelial growth factor-induced ICH is associated with increased MMP-9 expression. Suppression of MMP-9 by minocycline or pyrrolidine dithiocarbamate attenuated ICH, suggesting the therapeutic potential of MMP inhibitors in cerebral vascular rupture.

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Year:  2007        PMID: 17673717     DOI: 10.1161/STROKEAHA.106.481515

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  55 in total

1.  Minocycline improves functional outcomes, memory deficits, and histopathology after endovascular perforation-induced subarachnoid hemorrhage in rats.

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Review 2.  Neuroinflammatory mechanisms of blood-brain barrier damage in ischemic stroke.

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Review 3.  Roles of blood-brain barrier integrins and extracellular matrix in stroke.

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4.  Brain arteriovenous malformation pathogenesis: a response-to-injury paradigm.

Authors:  Helen Kim; Hua Su; Shantel Weinsheimer; Ludmila Pawlikowska; William L Young
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5.  Recombinant osteopontin attenuates brain injury after intracerebral hemorrhage in mice.

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6.  Reduced expression of integrin alphavbeta8 is associated with brain arteriovenous malformation pathogenesis.

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7.  Endothelial Notch4 signaling induces hallmarks of brain arteriovenous malformations in mice.

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Review 8.  Targeting reactive nitrogen species: a promising therapeutic strategy for cerebral ischemia-reperfusion injury.

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9.  Limb Ischemic Perconditioning Attenuates Blood-Brain Barrier Disruption by Inhibiting Activity of MMP-9 and Occludin Degradation after Focal Cerebral Ischemia.

Authors:  Changhong Ren; Ning Li; Brian Wang; Yong Yang; Jinhuan Gao; Sijie Li; Yuchuan Ding; Kunlin Jin; Xunming Ji
Journal:  Aging Dis       Date:  2015-11-17       Impact factor: 6.745

10.  Nitric oxide in vascular endothelial growth factor-induced focal angiogenesis and matrix metalloproteinase-9 activity in the mouse brain.

Authors:  Chanhung Z Lee; Zheng Xue; Qi Hao; Guo-Yuan Yang; William L Young
Journal:  Stroke       Date:  2009-06-04       Impact factor: 7.914

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