Granulocytic differentiation of HL-60 cells results in spontaneous apoptosis mediated by increased caspase expression
| Autor: | Jean Parodo, Richard Bitar, R.William G Watson, John C. Marshall, David J. Hackam, Ori D. Rotstein |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Neutrophils
Cellular differentiation Biophysics Retinoic acid Apoptosis HL-60 Cells Tretinoin Caspase 3 Cysteine Proteinase Inhibitors Biochemistry chemistry.chemical_compound Structural Biology Genetics medicine Humans Bcl-2 RNA Messenger fas Receptor Molecular Biology Caspase biology Caspase 1 Cell Differentiation Cell Biology Fas receptor Molecular biology Cell biology Cysteine Endopeptidases HL-60 Proto-Oncogene Proteins c-bcl-2 chemistry biology.protein Signal transduction Granulocytes Signal Transduction medicine.drug |
| Zdroj: | FEBS Letters. 412:603-609 |
| ISSN: | 0014-5793 |
| Popis: | HL-60 cells differentiating into neutrophil-like cells die an apoptotic death in vitro. Susceptibility to apoptosis is associated with decreased Bcl-2 protein and mRNA expression; however, the effect of differentiation on the expression of pro-apoptotic caspases is unknown. Spontaneous apoptosis occurred 6 days after retinoic acid treatment. Western blotting showed loss of Bcl-2 by day 7, and new expression of ICE (caspase 1) and CPP32 (caspase 3) protein by day 2. Northern analysis demonstrated loss of Bcl-2 mRNA and increases in ICE mRNA by day 2; CPP32 mRNA was unchanged. Differential Bcl-2 and ICE mRNA expression was also found when granulocytic differentiation was stimulated by DMSO. Differentiated HL-60 cell lysates exhibited functional ICE proteolytic activity. De novo caspase expression was responsible for the development of spontaneous apoptosis, since specific inhibitors of ICE (YVAD-CMK) and CPP32 (DEVD-CHO), inhibited retinoic acid induced spontaneous apoptosis. Functional maturation and susceptibility to apoptosis are both inducible and linked in this granulocyte precursor cell line. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|
Plný text