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Calcium and Fos Involvement in Brain‐Derived Ca 2+ ‐Binding Protein (S100)‐Dependent Apoptosis in Rat Phaeochromocytoma Cells
Author(s) -
Fulle Stefania,
Pietrangelo Tiziana,
Mariggiò Maria A.,
Lorenzon Paola,
Racanicchi Leda,
Mozrzymas Jerzy,
Guarnieri Simone,
ZucconiGrassi Gigliola,
Fanò Giorgio
Publication year - 2000
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1111/j.1469-445x.2000.01974.x
Subject(s) - apoptosis , immunocytochemistry , s100 protein , calcium in biology , calcium binding protein , calcium , microbiology and biotechnology , intracellular , biology , endocrinology , medicine , chemistry , biochemistry , immunohistochemistry , immunology
Brain‐derived calcium‐binding protein S100 induces apoptosis in a significant fraction of rat phaeochromocytoma (PC12) cells. We used single cell techniques (patch clamp, videomicroscopy and immunocytochemistry) to clarify some of the specific aspects of S100‐induced apoptosis, the modality(ies) of early intracellular Ca 2+ concentration increase and the expression of some classes of genes (c‐fos, c‐jun, bax, bcl‐x, p‐15, p‐21) known to be implicated in apoptosis of different cells. The results show that S100: (1) causes an increase of [Ca 2+ ] i due to an increased conductance of L‐type Ca 2+ channels; (2) induces a sustained increase of the Fos levels which is evident since the first time point tested (3 h) and remains elevated until to the last time point (72 h). All these data suggest that S100‐derived apoptosis in PC12 cells may be the consequence of a system involving an increase in L‐type Ca 2+ channel conductance with consequent [Ca 2+ ] i increase which up‐regulates, directly or indirectly, the expression of Fos.