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Endoplasmic reticulum may not be involved in the lead‐induced apoptosis in PC 12 cells in vitro
Author(s) -
Xu Jin,
Ji LinDan,
Xu LiHong
Publication year - 2010
Publication title -
environmental toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.813
H-Index - 77
eISSN - 1522-7278
pISSN - 1520-4081
DOI - 10.1002/tox.20474
Subject(s) - endoplasmic reticulum , apoptosis , microbiology and biotechnology , chop , mitochondrion , stim1 , unfolded protein response , calpain , chemistry , biology , biochemistry , enzyme
Recent researches indicated that mitochondrial pathway might play an important role in lead‐induced apoptosis. Our previous study also found that lead could induce apoptosis in PC 12 cells, and mitochondrial pathway events were involved in this process. As lead can disturb Ca 2+ homeostasis, the present study was undertaken to determine whether lead can activate key cellular events in the endoplasmic reticulum (ER) pathway, including the expressions of C/EBP homology protein (CHOP) and glucose‐regulated protein 78 (GRP78), and the activation of caspase‐12 and calpain. The results showed that lead could increase the expression of GRP78, while the expressions of CHOP and procaspase‐12 remained unchanged. Moreover, the caspase‐12 and calpain were not activated, and the ultrastructure of endoplasmic reticulum was not altered. Therefore, it suggests that lead may induce apoptosis in PC 12 cells through mitochondrial pathway, but not through the endoplasmic reticulum pathway. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2010.