Dc. Shields et al., Calpain activity and expression increased in activated glial and inflammatory cells in penumbra of spinal cord injury lesion, J NEUROSC R, 61(2), 2000, pp. 146-150
Following traumatic injury of the spinal cord, cells adjacent to the lesion
are subject to ischemic cell death as a result of vascular disruption and
secondary inflammatory responses. Proteases such as calcium-activated neutr
al proteinase (calpain) have been implicated in axon and myelin destruction
following injury since they degrade structural proteins in the axon-myelin
unit. To examine the role of calpain in cell death following spinal cord i
njury (SCI), calpain activity and translational expression were evaluated u
sing Western blotting techniques. Calpain activity (as measured by specific
substrate degradation) was significantly increased in and around the lesio
n site as early as 4 hr following injury with continued elevation at 48 hr
compared to sham controls. Likewise, calpain expression was significantly i
ncreased in both the lesion site and penumbra at 4 and 48 hr after injury.
Using double immunofluorescent labeling for calpain and cell-specific marke
rs, this increase in calpain expression was found to be due in part to acti
vated glial/inflammatory cells such as astrocytes, microglia, and infiltrat
ing macrophages in these areas. Thus, since calpain degrades many myelin an
d axonal structural proteins, the increased activity and expression of this
enzyme may be responsible for destruction of myelinated axons adjacent to
the lesion site following SCI. (C) 2000 Wiley-Liss, Inc.