Zinc deficiency affects T lymphocyte activity depending on the PKC isoenzyme pattern displayed in the studied cell type

PAULAZO M.A., ORQUEDA A., KLECHA A.J., BARREIRO ARCOS M.L., CREMASCHI G.A.

Buenos Aires, Argentina

Congreso; XXXIX Reunión Anual de la Sociedad Argentina de Farmacología Experimental; 2007

Sociedad Argentina de Farmacología Experimental

We have shown that zinc depletion in mitogen stimulated-T cell cultures lead to the inhibition of cell proliferation through a decrease in PKC isoenzymes crucial for T cell activation. To understand zinc actions on these signaling proteins, the effect of its deficit was analyzed in LBC and BW 5147 (BW) T cells that mainly expressed conventional and atypical PKC isoforms respectively. These cells were cultured in the absence or presence of specific intra-(TPEN) or extracellular (DTPA) Zn chelators and proliferation, PKC activity and the pattern of PKC isoenzymes were evaluated. Both chelators inhibited LBC cell proliferation, effect reverted by Zn addition. BW growth was not affected by Zn chelators. In both cell lines chelators affected PKC activity. DTPA decreased PKC q and TPEN diminished PKC a in LBC cells, while both chelators decrease a, but exerted no effect on the atypical PKC z isoform in BW cells. These results show that Zn actions on T cell proliferation, depend on the PKC isoenzyme pattern of the T cell type. Thus, Zn deficiency affect only T cells (normal and LBC cells), whose proliferation depends on novel or conventional isoforms, with two zinc-finger structures in their regulatory site, with no action on BW cells expressing the atypical PKC isoform.