Ionic regulation of MEL cell commitment.
A key event in the initiation of the dimethyl sulfoxide (DMSO)-induced program of murine erythroleukemia (MEL) cell differentiation is a rise in the level of cytoplasmic calcium ions. Our interest in the present study is whether other inducers of the terminal erythroid differentiation program also act via a calcium-dependent pathway. Inhibition of calcium transport has been found to prevent the induction of MEL cell commitment by DMSO, butyric acid (BA), or hypoxanthine (HX). Enhancement of the calcium flux rate with A23187 or elevation of cytoplasmic calcium levels with FCCP stimulates the kinetics of commitment in response to all three inducers. These results suggest that of the inducers we have tested (DMSO, BA, and HX), all three act to initiate commitment via a common mechanism which involves modulation of cytoplasmic calcium levels.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002087:Butyrates / Q000494:pharmacology; D020148:Butyric Acid; D002118:Calcium / Q000378:metabolism*; D002454:Cell Differentiation / Q000187:drug effects; D002460:Cell Line; D003593:Cytoplasm / Q000378:metabolism; D004121:Dimethyl Sulfoxide / Q000494:pharmacology; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000494:pharmacology; D004915:Leukemia, Erythroblastic, Acute / Q000378:metabolism* / Q000473:pathology; D007942:Leukemia, Experimental / Q000378:metabolism; D051379:Mice; D008928:Mitochondria / Q000378:metabolism
D002087:Butyrates; D007042:Hypoxanthines; D020148:Butyric Acid; D019271:Hypoxanthine; D002118:Calcium; D004121:Dimethyl Sulfoxide