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Arachidonate distribution in resting and proliferating primary human T cells
Author(s) -
Robichaud Philippe Pierre,
Boulay Katherine,
Poirier Samuel,
Surette Marc E
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1039.3
Subject(s) - cell growth , cell , phospholipid , chemistry , phosphatidylcholine , cell cycle , enzyme , microbiology and biotechnology , biology , biochemistry , membrane
Arachidonate‐phospholipid remodelling is characterised by the transfer of arachidonate (AA) between cellular phosphatidylcholine (PC) and phosphatidylethanolamine (PE) species. It has been suggested that AA‐phospholipid remodelling may control cellular AA distribution and availability. In this study, the cellular distribution of AA was measured in resting and in anti‐CD3+IL‐2 ‐stimulated primary human T cells. In pulse‐chase experiments a very rapid redistribution of [ 3 H]AA from PC to PE was measured in stimulated proliferating cells compared to resting cells. This increased remodelling was accompanied by a marked shift in the mass distribution of AA into 1‐alkyl‐ and 1‐alk‐1‐enyl‐linked PE species in stimulated cells. Minor differences in AA distribution were measured in cells arrested in different phases of the cell cycle (G1/S, G2/M and S), with the most marked changes observed when the cells transitioned from G0 into the cell cycle. The re‐distribution of AA in proliferating T cells was reversed when the stimulus was removed and the cells ceased to proliferate. Previous studies linked the expression of group IVC phospholipase A 2 with a redistribution of AA into PE species suggesting a role for this enzyme in remodelling. However, remodelling activity was not modified in HEK293 cells overexpressing this enzyme, suggesting that a different isozyme is likely involved. Microarray experiments are now underway with the aim of identifying which enzymes are possibly involved in the remodelling of arachidonate in cycling human T cells. (Supported by the Canadian Institutes of Health Research and the Canada Research Chairs Program).