Caspase involvement in the mitochondrial membrane depolarization during ganglioside-induced apoptosis of thymocytes View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2007-06

AUTHORS

R. V. Kholodenko, I. V. Kholodenko, N. Yu. Viskova, N. I. Lutsan, I. M. Molotkovskaya

ABSTRACT

Ganglioside-induced apoptosis in mouse thymocytes was shown to be caspase-dependent, mitochondria being involved in the apoptosis-signaling pathway of GM1-, GD3-and GT1b-stimulated cells. According to their role in caspase-8-induced signaling cascades in thymocytes, these gangliosides can be divided into two groups, viz., those activating cell apoptosis by a mitochondrial route without the involvement of death receptors and caspase-8 (the so-called mitochondrial signaling cascade) (GD3), and those activating this process by receptor-mediated and mitochondrial routes (GM1 and GT1b). Anti-Fas antibodies that activate apoptosis of thymocytes by receptor pathway were used as a reference system. Cytofluorimetric studies of chromosomal DNA fragmentation revealed that effector caspase-3 is involved in apoptotic signaling cascades triggered by all the gangliosides under study. At the same time, the caspase-3 inhibitor Z-DEVD-FMK abolished the ganglioside-and antibody-induced depolarization of thymocyte mitochondrial membranes by a receptor-dependent route either partly (GM1 and GT1b) or completely (anti-Fas antibodies). Thymocytes stimulated by GD3 by a mitochondrial apoptotic route were an exception. Possible mechanisms of the caspase-3 involvement in the regulation of the activity of mitochondrial apoptosis-induced channels (MAC) are discussed and in particular, the role of proapoptotic proteins Bax/Bid. More... »

PAGES

138-144

Identifiers

URI

http://scigraph.springernature.com/pub.10.1134/s1990747807020067

DOI

http://dx.doi.org/10.1134/s1990747807020067

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1053622571


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