Actin-depolymerizing factor (ADF)/
cofilin is a small cytoskeletal
protein that is a stimulus-responsive mediator of actin dynamics. ADF/
cofilin also translocates into mitochondria and nuclei in response to apoptotic stimuli for
cytochrome c release. These ADF/
cofilin translocations are negatively regulated by phosphorylation. Recently, it has been reported that pyridoxal-5'-phosphate (PLP)
phosphatase/chronophin (PLPP/CIN) regulates phosphorylation of ADF/
cofilin levels. Therefore, we investigated whether PLPP/CIN contributes to apoptosis-like events via modulation of ADF/
cofilin phosphorylation following
status epilepticus (SE). In the present study, apoptosis-like astroglial damages were detected in the dentate gyrus after SE. Upregulation of ADF/
cofilin and PLPP/CIN expression in the cytoplasm and nucleus were accompanied by apoptosis-like events. PLPP/CIN level showed a direct proportionality to nuclear translocation of ADF/
cofilin. Moreover, nuclear accumulation of
apoptosis-inducing factor was simultaneously observed with that of ADF/
cofilin. Tat-PLPP/CIN pretreatment accelerated astroglial apoptosis-like degeneration following SE, although Tat-PLPP/CIN transduction alone could not induce apoptosis or
necrosis in astrocytes. Therefore, our findings suggest that nuclear accumulation of ADF/
cofilin itself may not induce apoptogenic events, but may play a synergic role in apoptosis-like astroglial loss following SE.