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Antibody‐mediated glycophorin C coligation on K 562 cells induces phosphatidylserine exposure and cell death in an atypical apoptotic process
Author(s) -
Wang Duncheng,
Seto Eva,
Shu Jenny,
Micieli Jonathan A.,
Fernandes Bernard J.,
Denomme Gregory A.
Publication year - 2013
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1111/trf.12028
Subject(s) - glycophorin , propidium iodide , apoptosis , flow cytometry , phosphatidylserine , annexin , microbiology and biotechnology , biology , viability assay , cell growth , antigen , chemistry , programmed cell death , immunology , biochemistry , phospholipid , membrane
Background Glycophorin C ( GPC ) is necessary in the maintenance of red blood cell structure. Severe autoimmune hemolytic anemia and hemolytic disease of the fetus and newborn ( HDFN ) have been associated with G erbich ( G e) blood group system antigens expressed on GPC . Previous in vitro studies with cord blood progenitor cells have shown that anti‐ G e suppresses erythropoiesis. Study Design and Methods Here, we evaluated the K 562 erythroleukemic cell line to study the cellular effects of a murine anti‐ GPC . Cell proliferation was evaluated after treatment with anti‐ GPC . Flow cytometry was used to evaluate exofacial phosphatidylserine ( PS ) expression and cell viability (propidium iodide binding). Cell morphology was evaluated under light microscopy with cytospin preparations stained with M ay‐ G rünwald G iemsa. Results Anti‐ GPC dramatically inhibited K 562 proliferation and increased PS expression, consistent with cytoplasmic blebbing, suggesting evidence of apoptosis. Z ‐ VAD‐FMK , an inhibitor of classical apoptosis, was unable to reverse the suppressive effect of anti‐ GPC . However, hemin was able to attenuate growth suppression. Conclusion Together, the data suggest that anti‐ GPC suppresses erythroid proliferation through the induction of nonclassical apoptosis.