The AMP-activated protein kinase beta 1 subunit modulates erythrocyte integrity

- Prkab1tm1b/tm1b mice were generated and phenotyped.
- Prkab1tm1b/tm1b mice presented with microcytic anemia.
- Erythrocytes lacking Prkab1 have a variable morphologic appearance.
- Prkab1-deficient erythrocytes have increased osmotic resistance.
- The importance of the beta 1 isoform in erythrocyte integrity is discussed.

Failure to maintain a normal in vivo erythrocyte half-life results in the development of hemolytic anemia. Half-life is affected by numerous factors, including energy balance, electrolyte gradients, reactive oxygen species, and membrane plasticity. The heterotrimeric AMP-activated protein kinase (AMPK) is an evolutionarily conserved serine/threonine kinase that acts as a critical regulator of cellular energy balance. Previous roles for the alpha 1 and gamma 1 subunits in the control of erythrocyte survival have been reported. In the work described here, we studied the role of the beta 1 subunit in erythrocytes and observed microcytic anemia with compensatory extramedullary hematopoiesis together with splenomegaly and increased osmotic resistance.