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Hypothetical Model for the Suppression of Stress Induced Apoptosis in Hematopoietic Stem Cells by Bcl-2 Mutants
@Contributed equally to this manuscript.
*Dr. B. R. Ambedkar Centre for Biomedical Research
#INMAS, Delhi
Correspondence to: Gurudutta Gangenahalli, PhD Stem Cell Gene Therapy Research Group (INMAS), Lucknow Road, Timar Pur, Delhi-110054, Phone: 011-91-23911712, Fax: 011-91-25737049 e-mail: gugdutta@rediffmail.com
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This article was originally published by Wolters Kluwer - Medknow and was migrated to Scientific Scholar after the change of Publisher.
Abstract
Hematopoietic stem cells (HSC), which are responsible for maintaining continuous pool of blood cells, are being used for bone marrow transplantation (BMT). However, the programmed cell death/ apoptosis poses a serious problem for their optimum proliferation and differentiation after radio- and/ or chemotherapy. The role of Bcl-2 (B Cell Lymphoma) protein, a Bcl-2 family member, is well established in suppressing apoptosis of HSC on irradiation and serum withdrawal. The anti-apoptotic activity of Bcl-2 is regulated by inter- and intra-family homo-/ heterodimerization. Here we are proposing that the potential of Bcl-2 and its survival enhancing mutants, such as D34A and S70E, may be harnessed (gene therapy) to suppress the radiation and growth factor withdrawal induced apoptosis provided the neoplastic outcomes of these genes are regulated. The suggested hypothetical model is likely to be helpful in treating blood borne disorders and radiation injury through BMT.
