Affiliations: Hemorheology Center, Department of Medical Physics, School of Basic medical Sciences, Peking University, Health Science Center, Beijing 100083, China | Department of Bioengineering, University of California, San Diego, La Jolla, CA 92093‐0412, USA
Note: [] Corresponding author: Prof. Zong‐yao Wen, Hemorheology Center, Department of Medical Physics, Peking University, Health Science Center, Beijing 100083, P.R. China. Tel.: (8610)82802419; Fax: (8610)62015582; E‐mail: [email protected].
Abstract: Mutant p53 gene and wild‐type p53 gene were introduced into murine erythroleukemia cell line (MEL). The MEL cells transfected with mutant p53 gene (MEL‐M) and with wild‐type p53 gene (MEL‐W) were obtained by G418 selection. MEL, MEL‐W and MEL‐M were injected intraperitoneally into BALB/C mice. In the first week after injection, the signs of erythroleukemia were induced in all three groups. Abnormalities were mainly found in the spleen, bone marrow, liver and peripheral blood. There was an increase of proerythroblasts in the bone marrow. A large amount of normoblasts (early and intermediate erythroblasts) appeared in the spleen. In the peripheral blood, the white blood cells, reticulocyte and platelet counts increased and RBC count and hematocrit decreased. The degree of abnormalities in the MEL‐W group was significantly lower than that in other two groups. Hemorheological measurements indicated that the deformability and orientation of RBCs in MEL and MEL‐M groups were impaired, whereas those in MEL‐W group did not change significantly. Micropipette aspiration measurement revealed that MEL‐W had higher elastic modulus than MEL and MEL‐M, indicating that it was more difficult for MEL‐W to deform and migrate in vivo. The results of animal test and micropipette suggest that exogenous wild‐type p53 gene could reduce the tumorigenesis of murine erythroleukemia cells.
