Effect of Bcl-2 and caspase-3 on calcium distribution in apoptosis of HL-60 cells.
Cell Res
; 10(3): 213-20, 2000 Sep.
Article
en En
| MEDLINE
| ID: mdl-11032173
ABSTRACT
Apoptosis manifests in two major execution programs downstream of the death signal the caspase pathway and organelle dysfunction. An important antiapoptosis factor, Bcl-2 protein, contributes in caspase pathway of apoptosis. Calcium, an important intracellular signal element in cells, is also observed to have changes during apoptosis, which maybe affected by Bcl-2 protein. We have previously reported that in Harringtonine (HT) induced apoptosis of HL-60 cells, there's a change of intracellular calcium distribution, moving from cytoplast especially Golgi's apparatus to nucleus and accumulating there with the highest concentration. We report here that caspase-3 becomes activated in HT-induced apoptosis of HL-60 cells, which can be inhibited by overexpression of Bcl-2 protein. No sign of apoptosis or intracellular calcium movement from Golgi's apparatus to nucleus in HL-60 cells overexpressing Bcl-2 or treated with Ac-DEVD-CHO, a specific inhibitor of caspase-3. The results indicate that activated caspase-3 can promote the movement of intracellular calcium from Golgi's apparatus to nucleus, and the process is inhibited by Ac-DEVD-CHO (inhibitor of caspase-3), and that Bcl-2 can inhibit the movement and accumulation of intracellular calcium in nucleus through its inhibition on caspase-3. Calcium relocalization in apoptosis seems to be irreversible, which is different from the intracellular calcium changes caused by growth factor.
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Colección:
01-internacional
Banco de datos:
MEDLINE
Asunto principal:
Calcio
/
Apoptosis
/
Células HL-60
/
Proteínas Proto-Oncogénicas c-bcl-2
/
Caspasas
Límite:
Humans
Idioma:
En
Revista:
Cell Res
Año:
2000
Tipo del documento:
Article
País de afiliación:
China