Recent studies on cerebral
ischemic stroke have demonstrated the importance of the inflammatory response. Ongoing inflammatory insults have been implicated as a secondary mechanism underlying neuronal injury induced by
ischemia, and anti-inflammatory strategies have gained considerable interest.
Selenoprotein S (SelS), which is an endoplasmic reticulum resident
protein, is known to promote cell survival by regulating
inflammation. Moreover, SelS has been shown to be responsive to
ischemia in cultured astrocytes. A Finnish report revealed that a variation in the SelS gene locus is associated with a higher predisposition to
ischemic stroke in humans, suggesting a crucial role for SelS in protection against
brain ischemia. However, the time-course of SelS expression following
cerebral ischemia in vivo remains unknown. In the present study, we show, for the first time, differential SelS expression from 3 h to 7 days after reperfusion in rats with transient focal
cerebral ischemia induced by a 1-h
middle cerebral artery occlusion. We found that the SelS
protein level decreased in the ischemic core 3-7 days after reperfusion. Furthermore, SelS expression was upregulated in the ischemic penumbra adjacent to the ischemic core 3-7 days after reperfusion and is matched by reactive
astrogliosis. Thus, we propose that the upregulation of Sels represents a reaction of astrocytes against inflammatory stimuli, and the findings of this study open a new chapter in the research of the interrelationships between SelS and cerebral
ischemic stroke.