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BCL‐2‐Related Protein Expression in Apoptosis: Oxidative Stress Versus Serum Deprivation in PC12 Cells
Author(s) -
Maroto Rosario,
PerezPolo J. Regino
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.69020514.x
Subject(s) - apoptosis , nerve growth factor , dna fragmentation , oxidative stress , biology , microbiology and biotechnology , programmed cell death , bcl 2 family , bax protein , bcl xl , blot , endocrinology , medicine , protein expression , biochemistry , gene , receptor
Expression of the BCL‐2 protein family members, BAX, BAK, BAD, BCL‐xL, BCL‐xS, and BCL‐2, was measured (by western blotting using specific antibodies) in PC12 cells before and during apoptosis induced by either H 2 O 2 treatment or by serum deprivation and during rescue from apoptosis by nerve growth factor (NGF). H 2 O 2 ‐induced apoptosis, as measured by DNA fragmentation, caused: (a) a dose‐dependent increase in BAX, (b) a dose‐independent increase in BAK, and (c) a dose‐dependent inhibition of BAD expression. By comparison, apoptosis induced by serum deprivation resulted in a time‐dependent decrease in both BAX and BAK, along with a dramatic and sudden decrease in BAD expression. However, when PC12 cells were incubated in an apoptosis‐sparing medium (i.e., NGF‐supplemented serum‐free medium), both BAX and BAK were increased significantly, whereas BAD expression remained inhibited. BCL‐xL expression was increased by H 2 O 2 but unaffected by serum deprivation or long‐term NGF treatment. Neither BCL‐2 nor BCL‐xS expression could be detected in PC12 cells under the experimental conditions tested. Our results show that the expression of BAX, BAK, BAD, and BCL‐xL is altered in a stimulus‐dependent manner but cannot be used to define whether a cell will undergo or survive apoptosis. The similarity between changes in expression of BCL‐2‐related proteins induced by H 2 O 2 exposure and NGF rescue could reflect activation in part of a common antioxidant pathway.