Tubulin pools in human erythrocytes: altered distribution in hypertensive patients affects Na+,K+-ATPase activity

AMAIDEN, M.R.; SANTANDER, V.S; MONESTEROLO, N.E.; CAMPETELLI, A.N.; RIVELLI, J.F.; PREVITALI, G.; ARCE, C.A.; CASALE, C.H.

CELLULAR AND MOLECULAR LIFE SCIENCES

BIRKHAUSER VERLAG AG

Año: 2011 vol. 68 p. 1755 - 1768

1420-682X

The presence of tubulin in human erythrocytes was demonstrated using antibodies against total á-tubulin and different tubulin isotype. Tubulin was found to be distributed within the erythrocyte normal subjets (NS) in three distinct pools: membrane, sedimentable structure and soluble fraction. Erythrocytes from hypertensive subjets (HS) has inhibited the Na+,K+-ATPase (NKA) activity. The present study show that, in erythrocytes from HS, tubulin in the membrane is increased by ~150% compared to NS. Similar increases were observed for different tubulin isotype and for acetylated tubulin/NKA complex. Treatment of erythrocytes from NS with the microtubule-stabilizing agent taxol caused enhancement of acetylated tubulin in the membrane and inhibition of NKA activity, whereas treatment of erythrocytes from HS with the drug nocodazol cause the opposite effect of taxol. These results suggest that, in erythrocytes from HS, tubulin is translocated from the sedimentable to the membrane, where it associates with NKA and inhibits the enzyme activity.á-tubulin and different tubulin isotype. Tubulin was found to be distributed within the erythrocyte normal subjets (NS) in three distinct pools: membrane, sedimentable structure and soluble fraction. Erythrocytes from hypertensive subjets (HS) has inhibited the Na+,K+-ATPase (NKA) activity. The present study show that, in erythrocytes from HS, tubulin in the membrane is increased by ~150% compared to NS. Similar increases were observed for different tubulin isotype and for acetylated tubulin/NKA complex. Treatment of erythrocytes from NS with the microtubule-stabilizing agent taxol caused enhancement of acetylated tubulin in the membrane and inhibition of NKA activity, whereas treatment of erythrocytes from HS with the drug nocodazol cause the opposite effect of taxol. These results suggest that, in erythrocytes from HS, tubulin is translocated from the sedimentable to the membrane, where it associates with NKA and inhibits the enzyme activity.