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Interleukin-1beta mediates LPS-induced inhibition of apoptosis in retinoic acid-differentiated HL-60 cells.

Marshall JC, Jia SH, Parodo J, Watson RW

Department of Surgery, St. Michael's Hospital, University of Toronto, 4th Floor Bond Wing, Room 4-007, 30 Bond Street, Toronto, Ont., Canada.

Promyelocytic HL-60 cells differentiated to a neutrophilic phenotype by incubation with all-trans retinoic acid become constitutively apoptotic. Exposure to either LPS or IL-1beta inhibited the apoptosis of differentiated HL-60 cells. LPS induced the expression of pro-IL-1beta message, upregulated the activity of the interleukin-1beta converting enzyme (caspase-1), and increased the release of IL-1beta into the culture medium. Prevention of IL-1beta translation with an anti-sense oligonucleotide, or prevention of IL-1beta cellular binding with a blocking antibody, accelerated rates of spontaneous apoptosis, and abrogated the inhibitory effects of LPS. However inhibition of caspase-1 activity further inhibited constitutive apoptosis of mature HL-60 cells. These studies provide further evidence of a complex regulatory pathway that modulates the expression of granulocyte apoptosis during inflammation, and point to a specific role for IL-1beta as an autocrine survival factor.

Published 25 March 2008 in Biochem Biophys Res Commun, 369(2): 532-8.
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