Apoptosis in FA cells
Bone marrow failure occurred in aplastic anemia including FA is believed to be the consequence of hematopoietic stem cells (HSCs) depletion, which can be resulted from apoptosis, senescence, or excessive differentiation of HSCs. We are interested in understanding how FA proteins function to prevent apoptosis of HSCs and progenitor cells. We and others have demonstrated that excessive apoptosis of FA hematopoietic cells induced by apoptogenic cytokines such as tumor necrosis factor alpha (TNF-alpha; which is overproduced in FA patients) may contribute to the pathophysiology of bone marrow failure frequently occurred in FA children. We are studying whether apoptosis of BM cells induced by TNF-alpha leads to stem cell depletion using primary BM cells from FA patients and knockout mice and to define the pathological role of TNF-alpha in FA stem cell defect.
Related Publications
Where possible, article titles are linked to an abstract of the article. Selected citations may also be linked to PDFs of the article available on a Journal's site. Depending on the Journal's publishing policy, you may need a subscription to download the PDF.
Zhang X, Li J, Sejas DP, Pang Q. (2005) Hypoxia-reoxygenation induces premature senescence in FA bone marrow hematopoietic cells. Blood 106:75-85.
Zhang, X., Li, J., Sejas, D.P. and Pang, Q. (2005) The ATM/p53/p21 pathway influences cell fate decision between apoptosis and senescence in reoxygenated hematopoietic progenitor cells. J. Biol. Chem. 280:19635-19640.
Zhang, X., Li, J., Sejas, D. P. Rathbun, K.R., Bagby, G.C. and Pang, Q. (2004) The FA proteins functionally interact with the protein kinase PKR. J. Biol. Chem., 279:43910-43919.
For further information regarding Dr. Pang's research, please contact Dr. Qishen Pang at 513-636-1152. For additional information about the Division of Experimental Hematology, please contact Dr. David Williams at 513-636-0364. The Division of Experimental Hematology can be found in Room 6529 of Location R (Research Foundation Building).
