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  • Title: Bcl-2 inhibits hydrogen peroxide-induced ER Ca2+ pool depletion.
    Author: Distelhorst CW, Lam M, McCormick TS.
    Journal: Oncogene; 1996 May 16; 12(10):2051-5. PubMed ID: 8668330.
    Abstract:
    The mechanism by which Bcl-2 inhibits apoptosis is unknown. The Bcl-2 protein is localized to intracellular membranes, including the endoplasmic reticulum (ER). The ER is the major intracellular reservoir of Ca2+ in non-muscle cells, sequestering Ca2+ for use in intracellular signaling, and is a prime target of oxidative damage. Because of the recent suggestion that Bcl-2 acts in an antioxidant pathway, we wondered whether Bcl-2 might protect the ER Ca2+ pool in cells exposed to reactive oxygen species. To test this hypothesis, we assessed the effect of hydrogen peroxide (H2O2) treatment on the ER Ca2+ pool in WEH17.2 cells, which do not express Bcl-2, and two stable transfectants, W.Hb13 and W.Hb12. The Bcl-2 level by Western blotting is 4-fold higher in W.Hb12 cells compared to W.Hb13 cells. The ER Ca2+ pool in H2O2-treated and untreated cells was measured according to the amount of Ca2+ mobilized from the ER lumen into the cytoplasm by thapsigargin (TG), a selective inhibitor of the ER (Ca2+)-ATPase. H2O2 treatment produced a significant reduction in the TG-mobilizable Ca2+ pool in WEH17.2 and W.Hb13 cells, but not in W.Hb12 cells, indicating that overexpression of Bcl-2 preserves the integrity of the ER Ca2+ pool in cells exposed to reactive oxygen species.
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