Premium
Matrix metalloproteinase–9 and spontaneous hemorrhage in an animal model of cerebral amyloid angiopathy
Author(s) -
Lee JinMoo,
Yin KeJie,
Hsin Idar,
Chen Shawei,
Fryer John D.,
Holtzman David M.,
Hsu Chung Y.,
Xu Jian
Publication year - 2003
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.10671
Subject(s) - cerebral amyloid angiopathy , matrix metalloproteinase , pathogenesis , intracerebral hemorrhage , amyloid (mycology) , extracellular matrix , genetically modified mouse , pathology , metalloproteinase , medicine , transgene , biology , microbiology and biotechnology , biochemistry , disease , gene , dementia , subarachnoid hemorrhage
We examined the potential role of the extra‐cellular matrix‐degrading enzyme, matrix metalloproteinase‐9 (MMP‐9), in the pathogenesis of cerebral amyloid angiopathy (CAA)‐induced spontaneous hemorrhage. The amyloid‐beta peptide (Aβ) induced the synthesis, release and activation of MMP‐9 in murine cerebral endothelial cells, resulting in increased extracellular matrix degradation. Furthermore, extensive MMP‐9 immunoreactivity was observed in CAA‐vessels with evidence of microhemorrhage in aged APPsw transgenic mice, but not detected in aged wild type or young APPsw mice. These results suggest that increased vascular MMP‐9 expression, stimulated by Aβ, may play a role in the pathogenesis of spontaneous intracerebral hemorrhage in patients with CAA. Ann Neurol 2003;54:000–000