title: F-actin depolymerization accelerates clasmatodendrosis via activation of lysosome-derived autophagic astroglial death.
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.
authors.affiliation: Department of Anatomy and Neurobiology, College of Medicine, Hallym University, Chunchon, Kangwon-Do 200-702, South Korea.
authors.forename: H J
authors.initials: HJ
authors.lastname: Ryu
authors.forename: J-E
authors.initials: JE
authors.lastname: Kim
authors.forename: S-I
authors.initials: SI
authors.lastname: Yeo
authors.forename: D-W
authors.initials: DW
authors.lastname: Kim
authors.forename: O-S
authors.initials: OS
authors.lastname: Kwon
authors.forename: S Y
authors.initials: SY
authors.lastname: Choi
authors.forename: T-C
authors.initials: TC
authors.lastname: Kang
mesh_terms: D000199:Actins / Q000378:metabolism*; D000818:Animals; D000970:Antineoplastic Agents / Q000494:pharmacology; D001253:Astrocytes / Q000166:cytology / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology*; D001343:Autophagy / Q000502:physiology*; D015415:Biomarkers / Q000378:metabolism; D019086:Bridged Bicyclo Compounds, Heterocyclic / Q000494:pharmacology; D016923:Cell Death / Q000502:physiology*; D047630:Depsipeptides / Q000494:pharmacology; D008247:Lysosomes / Q000378:metabolism*; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012640:Seizures / Q000139:chemically induced / Q000473:pathology; D053778:Thiazolidines / Q000494:pharmacology
chemical_list: D000199:Actins; D000970:Antineoplastic Agents; D015415:Biomarkers; D019086:Bridged Bicyclo Compounds, Heterocyclic; D047630:Depsipeptides; D053778:Thiazolidines; C057531:jasplakinolide; C037067:latrunculin A