摘要
An extract (G-INH) made from mature human granulocytes freshly isolated from normai blood causes human neutrophils to undergo apoptosis in vitro as shown by morphologic changes and by the typical ladder pattern of small DNA fragments noted on agarose gel electrophoresis of isolated DNA. Apoptosis occurs in from 20% to 30% of neutrophils over 24 hours of culture in vitro and the addition of G-INH to the medium causes a dose-related increase in the incidence of apoptosis. Heating G-INH at 60t for 30 minutes does not destroy its capacity to induce apoptosis but GM-CSF, G-CSF, and to a lesser extent IL-1β, antagonize this action. IL-3 does not diminish G-INH induced apoptosis of neutrophils. Substances, released from, mature neutrophils may participate in regulating the survival of other neutrophils, particularly in sites where the cells are in close proximity as in the marrow. Self destruction of post-mitotic neutrophils in marrow may thus represent an-other level at which regulation of cell production
An extract (G-INH) made from mature human granulocytes freshly isolated from normai blood causes human neutrophils to undergo apoptosis in vitro as shown by morphologic changes and by the typical ladder pattern of small DNA fragments noted on agarose gel electrophoresis of isolated DNA. Apoptosis occurs in from 20% to 30% of neutrophils over 24 hours of culture in vitro and the addition of G-INH to the medium causes a dose-related increase in the incidence of apoptosis. Heating G-INH at 60t for 30 minutes does not destroy its capacity to induce apoptosis but GM-CSF, G-CSF, and to a lesser extent IL-1β, antagonize this action. IL-3 does not diminish G-INH induced apoptosis of neutrophils. Substances, released from, mature neutrophils may participate in regulating the survival of other neutrophils, particularly in sites where the cells are in close proximity as in the marrow. Self destruction of post-mitotic neutrophils in marrow may thus represent an-other level at which regulation of cell production and output occurs. The capacity of GM- and G-CSF to protect neutrophils from apoptosis induced by G-INH would provide a means for reducing this kind of cell loss allowing for the prompt availability of functionally capable celis for export to the blood.
出处
《中国实验血液学杂志》
CAS
CSCD
1995年第4期355-363,共9页
Journal of Experimental Hematology
基金
Rothrock Research Fund in Hematology, The authors appreclate the assistance of supervising technicina, Linda Russ.
Ulrica Stenheimer-Caudle, Sandra Peffly, and Marie Hyde.