F-actin depolymerization accelerates clasmatodendrosis via activation of lysosome-derived autophagic astroglial death

作者：Ryu H J; Kim J E; Yeo S I; Kim D W; Kwon O S; Choi S Y^*; Kang T C

来源：Brain Research Bulletin, 2011, 85(6): 368-373.

DOI：10.1016/j.brainresbull.2011.05.007

• F-actin
• LAMP-1
• LC3-II
• Jasplakinolide
• Latrunculin A

Clasmatodendrosis is an irreversible astroglial degenerative change, which includes extensive swelling and vacuolization of cell bodies and disintegrated and beaded processes. Since alteration in F-actin level influences on the formation of vacuoles/vesicles during exocytosis/endocytosis in astrocytes, we investigated whether F-actin polymerization involves clasmatodendrosis in the rat hippocampus following status epilepticus (SE). In the present study, vacuoles in clasmatodendrotic astrocytes showed LAMP-1 and LC3-II (a marker for autophagy) immunoreactivity. These findings reveal that clasmatodendrosis may be lysosome-derived autophagic astroglial death. jasplakinolide (an F-actin stabilizer) infusion significantly decreased the size and the number of medium/large-sized vacuoles in each clasmatodendritic astrocyte accompanied by enhancement of phalloidin signals, as compared to vehicle-infusion. In contrast, latrunculin A (an F-actin-depolymerizing agent) infusion increased the size and the number of medium/large-sized vacuoles, which were dissociated adjacent to cell membrane. Therefore, our findings suggest that F-actin stabilization may inhibit lysosome-derived autophagic astroglial death during clasmatodendrosis.

• 出版日期2011-7-15