Reduced sodium pump activity in inositol-deficient HL-60 cells: No evidence of control by protein kinase C

• Published in: Biochimica et biophysica acta Vol. 1220; no. 1; pp. 66 - 68
• Main Authors: Allard, Julien, Lennon, David P.W., Greenwood, Mark R., Buckenham, Alison J., Hawthorne, John N.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 16.12.1993; Elsevier Science
• Subjects: Analytical, structural and metabolic biochemistry; Biological and medical sciences; Cell physiology; Enzymes and enzyme inhibitors; Fundamental and applied biological sciences. Psychology; HL-60 cell; Humans; Hydrolases; Inositol; Inositol - metabolism; Membrane and intracellular transports; Molecular and cellular biology; Ouabain - pharmacology; Protein kinase C; Protein Kinase C - metabolism; Rubidium - metabolism; Sodium pump; Sodium-Potassium-Exchanging ATPase - metabolism; Tumor Cells, Cultured; Inositol; Protein kinase C; 12- O-tetra-decanoylphorbol-13-acetate; TPA; DMSO; dimethylsulfoxide; HL-60 cell; Sodium pump; Human; Promyelocytic leukemia; Regulation(control); Na; Membrane pump; Enzyme; Hydrolases; exchanging ATPase; K; Mechanism of action
• ISSN: 0167-4889; 0006-3002; 1879-2596
• DOI: 10.1016/0167-4889(93)90098-A

HL-60 cells were cultured in normal and inositol-deficient media. The inositol-deficient cells showed reduced sodium pump activity, as measured by ouabain-sensitive 86Rb + uptake. The protein kinase C inhibitors staurosporine and H7 did not affect uptake in either normal or inositol-deficient cells. However, U73122, a steroidal inhibitor of phosphoinositidase C, inhibited uptake in both types of cells. Activators of protein kinase C had no effect on Rb + entry. The inositol deficiency is not considered to affect the sodium pump by a mechanism involving diacylglycerol and protein kinase C.