Differential modulation of cell cycle, apoptosis and PPARy2 gene expression by PPARy agonists ciglitazone and 9-hydroxyoctadecadienoic acid in monocytic cells

J.K.A. Hampel, L.M. Brownrigg, D. Vignarajah, Kevin Croft, Arunasalam Dharmarajan, Jacqueline Bentel, Ian Puddey, Bu Yeap

Research output: Contribution to journalArticle

25 Citations (Scopus)

Abstract

We sought to compare the effects of the thiazolidinedione ciglitazone with the endogenous fatty acid PPARγ agonists 9- and 13-hydroxyoctadecadienoic acid (9- and 13-HODE), in U937 monocytic cells. Ciglitazone and 9-HODE inhibited cell proliferation and all three agonists increased cellular content of C18:0 fatty acids. Ciglitazone and 13-HODE resulted in an increased percentage of cells in S phase and ciglitazone reduced the percentage of cells in G2/M phase of cell cycle, whilst 9-HODE increased the percentage of cells in G0/1 and reduced the fraction in S and G2/M phases. 9-HODE selectively induced apoptosis in U937 cells, and increased PPARγ2 gene expression. Induction of apoptosis by 9-HODE was not abrogated by the presence of the PPARγ antagonist GW9662. Synthetic (TZD) and endogenous fatty acid ligands for PPARγ, ciglitazone and 9- and 13-HODE, possess differential, ligand specific actions in monocytic cells to regulate cell cycle progression, apoptosis and PPARγ2 gene expression.
Original languageEnglish
Pages (from-to)283-293
JournalProstaglandins, Leukotrienes & Essential Fatty Acids
Volume74
Issue number5
DOIs
Publication statusPublished - 2006

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