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Volume 2012, Article ID 168050, 6 pages
Research Article

Reduced PKC 𝛼 Activity Induces Senescent Phenotype in Erythrocytes

1Advanced Centre for Treatment, Research and Education in Cancer, Tata Memorial Centre, Kharghar, Navi Mumbai 410610, India
2Department of Medical Oncology, Jaslok Hospital and Research Centre, Mumbai 400026, India

Received 13 June 2012; Accepted 26 July 2012

Academic Editor: Eitan Fibach

Copyright © 2012 Rukmini B. Govekar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


The molecular mechanism mediating expression of senescent cell antigen-aggregated or cleaved band 3 and externalized phosphatidylserine (PS) on the surface of aged erythrocytes and their premature expression in certain anemias is not completely elucidated. The erythrocytes with these surface modifications undergo macrophage-mediated phagocytosis. In this study, the role of protein kinase C (PKC) isoforms in the expression of these surface modifications was investigated. Inhibition of PKC 𝛼 by 30 μM rottlerin (R30) and 2.3 nM Gö 6976 caused expression of both the senescent cell marker-externalized PS measured by FACS analysis and aggregated band 3 detected by western blotting. In contrast to this observation, but in keeping with literature, PKC activation by phorbol-12-myristate-13-acetate (PMA) also led to the expression of senescence markers. We explain this antithesis by demonstrating that PMA-treated cells show reduction in the activity of PKC 𝛼 , thereby simulating inhibition. The reduction in PKC 𝛼 activity may be attributed to the known downregulation of PMA-activated PKC 𝛼 , caused by its membrane translocation and proteolysis. We demonstrate membrane translocation of PKC 𝛼 in PMA-treated cells to substantiate this inference. Thus loss of PKC 𝛼 activity either by inhibition or downregulation can cause surface modifications which can trigger erythrophagocytosis.