Brain trauma induces expression of diacylglycerol kinase ζ in microglia

Diacylglycerol kinase (DGK) is an enzyme which phosphorylates a second messenger diacylglycerol and consists of a family of isozymes that differ in terms of structural motifs, enzymological property, and cell and tissue distribution. One of the isozymes, DGK zeta was originally shown to be expressed in various kinds of neurons under physiological conditions. However, we unexpectedly found that under pathological conditions, such as cerebral infarction, DGK zeta-immunoreactivity is detected in non-neuronal cells, although it remained to be elucidated in detail which cell types are responsible for the induced expression of DGK zeta in this setting. To further elucidate functional implications of DGK zeta in non-neuronal cells we performed detailed immunohistochemical analysis of DGK zeta using rat brain cryoinjury model. As early as I h after cryoinjury, DGK zeta-immunoreactivity was greatly decreased in the afflicted cerebral cortex and almost disappeared in the necrotic core. On day 7 after cryoinjury, however, DGK zeta-immunoreactivity reappeared in this area. DGK zeta-immunoreactivity was clearly detected in Iba1-immunoreactive cells of an oval or ameboid shape in the scar region, which represent activated microglia and/or macrophages. on the other hand, DGK zeta-immunoreactivity was not detected in Iba1-immunoreactive, resting microglia of ramified and dendritic configuration in the intact cortex. Furthermore, DGK zeta-immunoreactive cells were also positive for a microglia marker GLUT5 in the scar region, but never for an astrocyte marker GFAP. Taken together, the present study reveals that DGK zeta is induced in activated microglia in brain trauma, suggesting the functional significance of DGK zeta in this process. (C) 2009 Elsevier Ireland Ltd. All rights reserved.