THE GENERATION OF H-1-NMR-DETECTABLE MOBILE LIPID IN STIMULATED LYMPHOCYTES - RELATIONSHIP TS CELLULAR ACTIVATION, THE CELL-CYCLE, AND PHOSPHATIDYLCHOLINE-SPECIFIC PHOSPHOLIPASE-C
Mf. Veale et al., THE GENERATION OF H-1-NMR-DETECTABLE MOBILE LIPID IN STIMULATED LYMPHOCYTES - RELATIONSHIP TS CELLULAR ACTIVATION, THE CELL-CYCLE, AND PHOSPHATIDYLCHOLINE-SPECIFIC PHOSPHOLIPASE-C, Biochemical and biophysical research communications, 239(3), 1997, pp. 868-874
Mobile Lipids detected using H-1-NMR in stimulated lymphocytes were co
rrelated with cell cycle phase, expression of the interleukin-2 recept
or alpha and proliferation to assess the activation status of the lymp
hocytes. Mobile lipid levels, IL-2R alpha expression and proliferation
increased after treatment with PMA and ionomycin. PMA or ionomycin st
imulation alone induced increased IL-2R alpha expressiom but not proli
feration, PMA- but not ionomycin-stimulation generated mobile lipid, T
reatment with anti-CD3 antibody did not increase IL-2R alpha expressio
n or proliferation but did generate increased amounts of mobile lipid,
The cell cycle status of thymocytes treated with anti-CD3, PMA or ion
omycin alone indicated an. accumulation of the cells in the G(1) phase
of the cell cycle, The generation of mobile lipid was abrogated in an
ti-CD3 antibody-stimulated thymic lymphocytes but not in splenic lymph
ocytes, using a phosphatidylcholine-specific phospholipase C (PC-PLC)
inhibitor which blocked cells in the G(1)/S phase of the cell cycle, T
his suggests that the H-1-NMR-detectable mobile Lipid may be generated
in anti-CD3 antibody-stimulated thymic lymphocytes by the action of P
C-PLC activity via the catabolism of PC, in the absence of classical s
igns of activation. (C) 1997 Academic Press.