Erythropoietin responses and physical characterization of erythroid progenitor cells in rauscher virus infected BALB/c mice

✍ Scribed by Suzanne Hasthorpe; Simon Bol

• Publisher: John Wiley and Sons
• Year: 1979
• Tongue: English
• Weight: 774 KB
• Volume: 100
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.1041000108

✦ Synopsis

Abstract

Infection of BALB/c mice with Rauscher leukemia virus (RLV) gives rise to pronounced erythrocytopoiesis manifesting in splenomegaly and is associated with progressive development of anemia. In the spleen erythroid colony forming units (CFU‐E) increase exponentially up to 800‐fold that of normal levels by the third week of infection. In vitro these CFU‐E are dependent on erythropoietin for colony formation, their erythropoietin requirements being higher than that of CFU‐E from normal mice. Numbers of CFU‐E in spleen and degree of splenomegaly in anemic RLV infected mice were also shown to be modified by red blood cell transfusion, but progression of the disease was not stopped. Erythroid burst forming units (BFU‐E) were also responsive to erythropoietin. However, a small proportion of cells also formed BFU‐E colonies at concentrations which did not support growth of normal marrow BFU‐E.

When compared to normal, CFU‐E found in RLV‐infected spleen have similar velocity sedimentation rates. However, buoyant density separation of leukemic spleen cells indicated that CFU‐E were more homogeneous (modal density 1.0695 g/cm^3^) than CFU‐E from normal spleen. Analysis of physical properties of CFU‐E and the nonhemoglobinized erythroblast‐like cells, which accumulate in the spleen showed that they differed mainly in their distribution of cell diameter.

Our findings show that erythroid progenitor cells in RLV infected mice are responsive to erythropoietin in vitro. Also in vivo erythropoiesis appears to be under control of erythropoietin but other factors which lead to progression of RLV disease apparently exist. Most proerythroblast‐like cells, which are characteristic of this disease, apparently lack the potential to form colonies and may be more mature than CFU‐E.