Differential matrix metalloproteinase expression in cases of multiple sclerosis and stroke
- 31 October 1997
- journal article
- Published by Wiley in Neuropathology and Applied Neurobiology
- Vol. 23 (5), 406-415
- https://doi.org/10.1111/j.1365-2990.1997.tb01315.x
Abstract
D.C. Anthony, B. Ferguson, M.K. Matyzak, K.M. Miller, M.M. Esiri and V.H. Perry (1997) Neuropathology and Applied Neurobiology23, 406–415 Differential matrix metalloproteinase expression in cases of multiple sclerosis and stroke Multiple sclerosis (MS) and stroke pathology are characterized by blood–brain barrier breakdown, leucocyte emigration, and tissue destruction. Each process is thought to involve the matrix metalloproteinases (MMP), but little is known of their expression. We undertook to investigate whether MMP expression is dependent on the nature of the CNS lesion and whether expression would coincide with the histopathology. MS or cerebral‐infarct tissue was examined for the presence of gelatinase‐A, gelatinase‐B, matrilysin and stromelysin‐1. Gelatinases A and B and matrilysin expression was found to be up‐regulated in microglia/macrophages within acute MS lesions. In active‐chronic MS lesions, matrilysin and gelatinase‐A expression was pronounced in the active borders. In chronic MS lesions, the expression of matrilysin was confined to macrophages within perivascular cuffs. The pattern of MMP expression in infarct lesions differed considerably. Gelatinase‐B was strongly expressed by neutrophils in tissue from patients up to 1 week after an infarct, whereas gelatinase‐A and matrilysin staining was much less marked. From 1 week to 5 years, neutrophils were absent and the large number of macrophages present were expressing matrilysin and gelatinase A. Only a low level of gelatinase‐A and matrilysin expression was observed in normal brain controls. Thus, MMPs are expressed in inflammatory lesions in the CNS, but their individual expression is dependent on the nature and chronicity of the lesion. However, the general pattern of expression, in perivascular cuffs and in active lesions, supports a role for these enzymes as mediators of blood–brain barrier breakdown and tissue destruction, both in MS and in cerebral ischaemia.Keywords
This publication has 41 references indexed in Scilit:
- Matrix metalloproteinase expression during experimental autoimmune encephalomyelitis and effects of a combined matrix metalloproteinase and tumour necrosis factor-α inhibitorJournal of Neuroimmunology, 1997
- The Expression of Tissue-type Plasminogen Activator, Matrix Metalloproteases and Endogenous Inhibitors in the Central Nervous System in Multiple SclerosisJournal of Neuropathology and Experimental Neurology, 1996
- Divergent regulation by growth factors and cytokines of 95 kDa and 72 kDa gelatinases and tissue inhibitors or metalloproteinases-1, -2, and -3 in rabbit aortic smooth muscle cellsBiochemical Journal, 1996
- Role of gelatinase B and elastase in human polymorphonuclear neutrophil migration across basement membrane.American Journal of Respiratory Cell and Molecular Biology, 1996
- Matrix metalloproteinases degrade myelin basic proteinNeuroscience Letters, 1995
- Inhibition of cartilage and bone destruction in adjuvant arthritis in the rat by a matrix metalloproteinase inhibitor.The Journal of Experimental Medicine, 1995
- Matrix metalloproteinases and processing of pro-TNF-αJournal of Leukocyte Biology, 1995
- Protease expression in experimental colitisInflammation Research, 1994
- BLOOD-BRAIN BARRIER DAMAGE IN ACUTE MULTIPLE SCLEROSIS PLAQUESBrain, 1991
- Purification of rabbit bone inhibitor of collagenaseBiochemical Journal, 1981