F-actin depolymerization accelerates clasmatodendrosis via activation of lysosome-derived autophagic astroglial death.
Brain Res Bull
; 85(6): 368-73, 2011 Jul 15.
Article
em En
| MEDLINE
| ID: mdl-21624438
ABSTRACT
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.
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Autofagia
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Astrócitos
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Actinas
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Morte Celular
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Lisossomos
Idioma:
En
Ano de publicação:
2011
Tipo de documento:
Article
País de afiliação:
Coréia do Sul