Stroke induces extensive tissue remodeling, resulting in the activation of several cell types in the brain as well as recruitment of blood-borne leucocytes.
Radixin is part of a cytoskeleton linker
protein family with the ability to connect transmembrane
proteins to the actin cytoskeleton, promoting cell functions involving a dynamic cytoskeleton such as morphological changes, cell division and migration which are common events of different cell types after
stroke. In the healthy adult brain
radixin is expressed in Olig2(+) cells throughout the brain and in neural progenitor cells in the subventricular zone. In the current study, we detected a 2.5 fold increase in the number of
radixin positive cells in the peri-
infarct cortex two weeks after the induction of cortical
stroke by photothrombosis. Similarly, the number of Olig2(+) cells increased in the peri-
infarct area after
stroke; however, the number of
radixin(+)/Olig2(+) cells was unchanged. Neural progenitor cells maintained
radixin expression on their route to the
infarct. More surprising however, was the expression of
radixin in activated microglia in the peri-
infarct cortex. Seventy percent of Iba1(+) cells expressed
radixin after
stroke, a population which was not present in the control brain. Furthermore, activation of
radixin was predominantly detected in the peri-
infarct region of oligodendrocyte progenitors and microglia. The specific location of
radixin(+) cells in the peri-
infarct region and in microglia suggests a role for
radixin in microglial activation after
stroke.