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J. Biol. Chem., Vol. 266, Issue 10, 6188-6194, Apr, 1991
D Boscoboinik, A Szewczyk, C Hensey and A Azzi
The effect of alpha-tocopherol (vitamin E) on the proliferation of vascular
smooth muscle cells (A7r5), human osteosarcoma cells (Saos-2), fibroblasts
(Balb/3T3), and neuroblastoma cells (NB2A) has been studied. The
proliferation of vascular smooth muscle cells was inhibited by
physiologically relevant concentrations of alpha- tocopherol, neuroblastoma
cells were only sensitive to higher alpha- tocopherol concentrations, and
proliferation of the other cell lines was not inhibited. The inhibition of
smooth muscle cell proliferation was specific for alpha-tocopherol. Trolox,
phytol, and alpha-tocopherol esters had no effect. Proliferation of smooth
muscle cells stimulated by platelet-derived growth factor or endothelin was
completely sensitive to alpha-tocopherol. If smooth muscle cells were
stimulated by fetal calf serum, proliferation was 50% inhibited by alpha-
tocopherol. No effect of alpha-tocopherol was observed when proliferation
of smooth muscle cells was stimulated by bombesin and lysophosphatidic
acid. The possibility of an involvement of protein kinase C in the cell
response to alpha-tocopherol was suggested by experiments with the isolated
enzyme and supported by the 2- to 3-fold stimulation of phorbol ester
binding induced by alpha-tocopherol in sensitive cells. Moreover,
alpha-tocopherol also caused inhibition of protein kinase C translocation
induced by phorbol esters and inhibition of the phosphorylation of its
80-kDa protein substrate in smooth muscle cells. A model is discussed by
which alpha-tocopherol inhibits cell proliferation by interacting with the
cytosolic protein kinase C, thus preventing its membrane translocation and
activation.
Inhibition of cell proliferation by alpha-tocopherol. Role of protein kinase C
Institut fur Biochemie und Molekularbiologie, Universitat Bern, Switzerland.
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