par Foretz, Marc;Guihard, Soizic;Leclerc, Jocelyne;Fauveau, Véronique;Couty, Jean-Pierre;Andris, Fabienne 
;Gaudry, Murielle;Andreelli, Fabrizio;Vaulont, Sophie;Viollet, Benoit
Référence FEBS letters, 584, 16, page (3667-3671)
Publication Publié, 2010-08
;Gaudry, Murielle;Andreelli, Fabrizio;Vaulont, Sophie;Viollet, BenoitRéférence FEBS letters, 584, 16, page (3667-3671)
Publication Publié, 2010-08
Article révisé par les pairs
| Résumé : | AMP-activated protein kinase (AMPK) plays a pivotal role in regulating cellular energy metabolism. We previously showed that AMPKα1-/- mice develop moderate anemia associated with splenomegaly and high reticulocytosis. Here, we report that splenectomy of AMPKα1-/- mice worsened anemia supporting evidence that AMPKα1-/- mice developed a compensatory response through extramedullary erythropoiesis in the spleen. Transplantation of bone marrow from AMPKα1-/- mice into wild-type recipients recapitulated the hematologic phenotype. Further, AMPKα1-/- red blood cells (RBC) showed less deformability in response to shear stress limiting their membrane flexibility. Thus, our results highlight the crucial role of AMPK to preserve RBC integrity. © 2010 Federation of European Biochemical Societies. |
