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Regulation of HL-60 Differentiation by Lipoxygenase Pathway Metabolites in Vitro¹

University of Florida, College of Medicine [A. M. M., S. M. K.] and the Veterans Affairs Medical Center [A. M. M., S. M. K., R. M.], Gainesville, Florida 32610

We have studied the effects of lipoxygenase inhibition and metabolite addition on HL-60 cells induced to differentiate. When HL-60 are induced by dimethyl sulfoxide (DMSO) in the presence of an inhibitor of lipoxygenase, caffeic acid, there is a marked change from the expected phenotype of mature granulocytes to a population composed predominantly of mature monocytes. (DMSO alone: 54% granulocytes, 10% monocytes; DMSO + caffeic acid: 23% granulocytes, 53% monocytes.) Addition of leukotriene D₄ to DMSO-induced, caffeic acid-inhibited cultures resulted in a dose-dependent recovery of the granulocyte phenotype. Addition of lipoxygenase inhibitors to phorbol ester-treated HL-60 cells did not alter the expected monocytic differentiation. These results support a role for leukotriene D₄ in the regulation of granulocyte differentiation of HL-60 cells induced with DMSO.

¹ Supported by Public Health Service Grant CA44838 awarded by the National Cancer Institute, the Department of Health and Human Services, and the Medical Research Service of the Department of Veterans Affairs. A. M. M is a recipient of an American Cancer Society Clinical Oncology Career Development Award. Leukotrienes used in this study were provided by the Upjohn Co., Kalamazoo, MI.

² To whom requests for reprints should be addressed, at Box J-277, J Hillis Miller Health Center, University of Florida College of Medicine, Gainesville, FL 32610.

Received 1/ 8/90. Accepted 8/ 9/90.

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