Pathophysiological role of calpain in experimental demyelination

Citation
Dc. Shields et Nl. Banik, Pathophysiological role of calpain in experimental demyelination, J NEUROSC R, 55(5), 1999, pp. 533-541
Citations number
76
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROSCIENCE RESEARCH
ISSN journal
03604012 → ACNP
Volume
55
Issue
5
Year of publication
1999
Pages
533 - 541
Database
ISI
SICI code
0360-4012(19990301)55:5<533:PROCIE>2.0.ZU;2-M
Abstract
Calcium-activated neutral proteinase (calpain) has been extensively studied over the past three decades such that many enzymatic and structural proper ties of this enzyme are well understood. However, the pathophysiological ro les of calpain remain poorly defined. In addition to recent studies delinea ting a role for calpain in various pathological conditions, this proteinase has been implicated in the degradation of myelin proteins in autoimmune de myelinating diseases such as multiple sclerosis and experimental allergic e ncephalomyelitis (EAE), In EAE, calpain translational expression is signifi cantly increased in activated glial/inflammatory cells that participate in myelinolysis while calpain substrates (axonal and myelin proteins) are lost . Thus, since all major myelin proteins are calpain substrates, early studi es suggest calpain may play an important role in demyelination of the centr al nervous system. (C) 1999 Wiley-Liss, Inc.