UNDERGRADUATE RESEARCH ASSISTANT UNIVERSITY OF IOWA IOWA CITY, Iowa, United States
Introduction/Rationale: Acute radiation syndrome (ARS) results from exposure to ionizing radiation during medical treatment, nuclear accidents, & space travel. A common side effect of ARS is bone marrow damage & anemia. Healthy red blood cells (RBCs) highly express CD47. A previous study has shown progressive decrease in CD47 expression by RBCs following radiation exposure, suggesting RBC damage & death. Preliminary data from our lab shows Cd47-/- mice are highly susceptible to radiation. Clearance of damaged RBCs is typically mediated by SIRPa expressing phagocytes following decrease in CD47 expression by RBCs. Recent work has revealed RBCs can also undergo programmed inflammatory cell death known as spectosis. To this end, we evaluated RBC death & morphology, as well as anemia following radiation in the absence of CD47.
Methods: We non-lethally irradiated C57BL/6, Cd47-/-, & Cd47-/-Sirpa-/- (DKO) mice. Mice were bled retroorbitally at multiple time points during the recovery period. We evaluated RBC morphology via blood smears, total white blood cells, RBCs, and complete blood counts.
Results: We observed slight anemia in Cd47-/- compared to controls, and even more exaggerated anemia in DKO. We also observed more morphological abnormalities in the absence of CD47 than in controls.
Conclusion: This data suggests that CD47 is required for efficient recovery of the hematopoietic compartment following radiation. This is a potential mechanism mediating susceptibility of Cd47-/- to ionizing radiation.
