RADIATION-ENHANCED DIFFERENTIATION OF ERYTHROID PROGENITOR CELLS AND ITS RELATION TO REPRODUCTIVE CELL-DEATH

Citation
K. Schwenke et al., RADIATION-ENHANCED DIFFERENTIATION OF ERYTHROID PROGENITOR CELLS AND ITS RELATION TO REPRODUCTIVE CELL-DEATH, International journal of radiation biology, 69(3), 1996, pp. 309-317
Citations number
39
Categorie Soggetti
Radiology,Nuclear Medicine & Medical Imaging","Nuclear Sciences & Tecnology
ISSN journal
09553002
Volume
69
Issue
3
Year of publication
1996
Pages
309 - 317
Database
ISI
SICI code
0955-3002(1996)69:3<309:RDOEPC>2.0.ZU;2-D
Abstract
Terminally differentiated cells usually do not divide and are, thus, r eproductively dead. To elucidate the significance of radiation-enhance d differentiation to reproductive cell death, murine erythroid progeni tor cells were gamma-irradiated in plasma clot cultures and the develo pment of haemoglobinized clones was studied thereafter. If irradiation occur-red when the cells had resumed proliferation, the total numbers of haemoglobinized clones and, in parallel, the numbers of newly haem oglobinized clones were elevated above control levels 6-24 h after 10- 30 Gy and 24-48 h after 1 Gy respectively. Thereafter, clone numbers d ecreased below controls. This decrease was faster with the newly haemo globinized clones, indicating that both the accumulation of haemoglobi nized clones and fast exhaustion of the pool of more primitive precurs ors in the cultures are due to accelerated differentiation. The haemog lobinized clones appearing after irradiation were reduced in size with out indication of direct cell death. We conclude that the reproductive cell death occurring in our system is due to enhancement of different iation. Enhancement of differentiation is expressed by omission of cel l cycles normally passed through by the cell progeny before terminal d ifferentiation is reached. Dependence of differentiation enhancement o n the presence of cycling cells at the time of irradiation indicates i nvolvement of growth of essential cytoplasmic constituents during mito tic delay as observed in other cell systems.