Inhibition of deoxygenation-induced membrane protein dephosphorylation and cell dehydration by phorbol esters and okadaic acid in sickle cells

• Published in: Blood Vol. 86; no. 5; pp. 1999 - 2007
• Main Authors: HASSANA FATHALLAH, COEZY, E, DE NEEF, R.-S, HARDY-DESSOURCES, M.-D, GIRAUD, F
• Format: Journal Article
• Language: English
• Published: Washington, DC The Americain Society of Hematology 01.09.1995
• Subjects: Adenosine Triphosphate - blood; Anemia, Sickle Cell - blood; Anemias. Hemoglobinopathies; Biological and medical sciences; Biological Transport; Calcium - blood; Calcium-Transporting ATPases - blood; Desiccation; Diseases of red blood cells; Erythrocyte Membrane - drug effects; Erythrocyte Membrane - metabolism; Erythrocytes - drug effects; Erythrocytes - physiology; Ethers, Cyclic - pharmacology; Hematologic and hematopoietic diseases; Humans; In Vitro Techniques; Kinetics; Medical sciences; Membrane Proteins - blood; Membrane Proteins - drug effects; Membrane Proteins - isolation & purification; Okadaic Acid; Oxygen - blood; Phosphates - blood; Phosphorus Radioisotopes; Potassium - blood; Protein Kinase C - metabolism; Protein Tyrosine Phosphatases - antagonists & inhibitors; Reference Values; Sodium - blood; Tetradecanoylphorbol Acetate - pharmacology; Human; Hemoglobinopathy; Phosphorylation; Hemolytic anemia; Sickle cell anemia; Sickle cell erythrocyte; Hemopathy; Dehydration; Genetic disease

Deoxygenation (DO) of sickle cell anemia red blood cells (SS cells) induces membrane permeabilization to Ca2+, Na+, and K+ and cell dehydration mostly through the activation of the Ca(2+)-dependent K+ channels. We show that DO of both SS cells and normal red blood cells was accompanied by a nonspeci...