Brain trauma induces expression of diacylglycerol kinase zeta 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, DGKzeta 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, DGKzeta-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 DGKzeta in this setting. To further elucidate functional implications of DGKzeta in non-neuronal cells we performed detailed immunohistochemical analysis of DGKzeta using rat brain cryoinjury model. As early as 1h after cryoinjury, DGKzeta-immunoreactivity was greatly decreased in the afflicted cerebral cortex and almost disappeared in the necrotic core. On day 7 after cryoinjury, however, DGKzeta-immunoreactivity reappeared in this area. DGKzeta-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, DGKzeta-immunoreactivity was not detected in Iba1-immunoreactive, resting microglia of ramified and dendritic configuration in the intact cortex. Furthermore, DGKzeta-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 DGKzeta is induced in activated microglia in brain trauma, suggesting the functional significance of DGKzeta in this process.