抄録
Jasplakinolide, a cell-permeable monocyclic peptide, binds to the F-actin and induces actin stabilization in vitro. In epithelial cells, actin filament network is important for the functions, because disruption of actin filament network causes morphological alteration, dissociation of mitosis and cell death. In salivary glands, actin filaments have been suggested to contribute to cell-cell adhesion, polarization and scaffold of plasma membrane. Apoptosis is a regulated process by which a cell undergoes a form of cell death characterized by DNA cleavage, nuclear condensation, cell shrinkage and membrane blebbing. We here demonstrate that jasplakinolide induces apoptosis in rat parotid acinar cells. Parotid acinar cells of male Sprague-Dawley rats were dispersed using trypsin and collagenase digestion. For morphological study, confocal and conventional transmission electron microscopies were used. DNA ladder was electrophoretically separated. When parotid acinar cells were treated with jasplakinolide, decrease of fluorescence intensity of submembrous F-actin was observed in fluorescence microscopy. In the cells, actin filament aggregation was elicited. In conventional transmission electron microscopy, chromatin aggregation, membrane blebbing and apoptotic bodies were observed exclusively in the jasplakinolide-treated cells. Jasplakinolide-induced apoptosis was confirmed by detection of DNA ladder and DNA fragmentation. Taken together, jasplakinolide induces apoptosis in rat parotid acinar cells. [Jpn J Physiol 54 Suppl:S83 (2004)]
