cytochrome-c-t has been researched along with Monosomy* in 1 studies
1 other study(ies) available for cytochrome-c-t and Monosomy
| Article | Year |
|---|---|
Antiapoptotic role of growth factors in the myelodysplastic syndromes: concordance between in vitro and in vivo observations.
Erythroid apoptosis in low-risk myelodysplastic syndrome (MDS) maybe mediated via mitochondrial release of cytochrome c and subsequent caspase activation. In the present study, we compared the in vitro and in vivo effects of proerythroid treatment with erythropoietin + granulocyte colony-stimulating factor (G-CSF) on myelodysplastic erythropoiesis regarding apoptosis and preferential growth of clones with cytogenetic abnormalities.. We enrolled 15 refractory anemia (RA) and 11 refractory anemia with ringed sideroblasts (RARS), including 5q- aberration, monosomy 7, and trisomy 8, before initiation of treatment and followed nine patients after successful treatment. The effects of G-CSF and erythropoietin were assessed. The expression of G-CSF receptor (G-CSFR) was explored during erythroid maturation. The relative growth of erythroid progenitors with cytogenetic aberrations in presence of erythropoietin was investigated.. Significant redistribution of cytochrome c was seen before treatment at all stages of erythroid differentiation. This release was blocked by G-CSF during the whole culture period and by erythropoietin during the latter phase. Both freshly isolated glycophorin A+ bone marrow cells and intermediate erythroblasts during cultivation retained their expression of G-CSFR. Cytochrome c release and caspase activation were significantly less pronounced in progenitors obtained from successfully treated nonanemic patients and showed no further response to G-CSF in vitro. Moreover, erythropoietin significantly promoted growth of cytogenetically normal cells from 5q- patients, whereas no such effect was observed on erythroblasts from monosomy 7 or trisomy 8 patients.. We conclude that growth factors such as erythropoietin and G-CSF can act both via inhibition of apoptosis of myelodysplastic erythroid precursors and via selection of cytogenetically normal progenitors. Topics: Adult; Aged; Aged, 80 and over; Anemia, Refractory; Anemia, Sideroblastic; Apoptosis; Bone Marrow Cells; Caspases; Cytochromes c; Enzyme Activation; Erythroid Precursor Cells; Erythropoietin; Glycophorins; Granulocyte Colony-Stimulating Factor; Humans; In Vitro Techniques; Middle Aged; Monosomy; Receptors, Granulocyte Colony-Stimulating Factor; Recombinant Proteins; Trisomy | 2005 |