Comparative proteomics of erythrocyte aging in vivo and in vitro

During aging in vivo and in vitro, erythrocytes display removal signals. Phagocytosis is triggered by binding of autologous IgG to a senescent cell antigen originating on band 3. Erythrocytes generate vesicles as an integral part of the aging process in vivo and in vitro, i.e. during storage. These...

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Published inJournal of proteomics Vol. 73; no. 3; pp. 396 - 402
Main Authors Bosman, G.J.C.G.M., Lasonder, E., Groenen-Döpp, Y.A.M., Willekens, F.L.A., Werre, J.M., Novotný, V.M.J.
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 03.01.2010
Subjects
Aging
Blood Banking - methods
Blood Banks - standards
Blood Preservation - methods
Blood Preservation - standards
Cells, Cultured
Cytoplasmic Vesicles - metabolism
Erythrocyte
Erythrocyte Aging - physiology
Erythrocyte Membrane - metabolism
Erythrocytes - chemistry
Erythrocytes - metabolism
Humans
Membrane
Proteomics - methods
Storage
Vesicles
Erythrocyte
Aging
Membrane
Vesicles
Storage
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Summary:During aging in vivo and in vitro, erythrocytes display removal signals. Phagocytosis is triggered by binding of autologous IgG to a senescent cell antigen originating on band 3. Erythrocytes generate vesicles as an integral part of the aging process in vivo and in vitro, i.e. during storage. These vesicles display senescent cell antigens as well as phosphatidylserine, that is recognized by scavenger receptors. Recent comparative proteomic analyses of erythrocytes and their vesicles support the hypothesis that aging is accompanied by increased binding of modified hemoglobins to band 3, disruption of the band 3-mediated anchorage of the cytoskeleton to the lipid bilayer, vesicle formation, and antigenic changes in band 3 conformation. Proteomic data also suggest an, until then unknown, involvement of chaperones, stress proteins, and proteasomes. Thus, the presently available comparative proteomic analyses not only confirm previous immunochemical and functional data, but also (1) provide new clues to the mechanisms that maintain erythrocyte homeostasis; (2) open new roads to elucidate the processes that regulate physiological erythrocyte aging and removal, and thereby; (3) provide the foundation for rational interventions to prevent untimely erythrocyte removal, and unwanted interactions between the erythrocyte and the immune system, especially after transfusion.
ISSN:1874-3919
1876-7737
DOI:10.1016/j.jprot.2009.07.010