Journal
GENERAL AND COMPARATIVE ENDOCRINOLOGY
Volume 166, Issue 2, Pages 241-249Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.ygcen.2009.08.011
Keywords
DEX; Calcium; Apoptosis; IP3R1; SERCA1; GRE
Categories
Funding
- National Key Technology R&D Program in the 11th Five Year Plan of China [2006BAD14B02-6, 2006BAD01A08-07]
- National 863 plans projects [2006AA10Z140]
- Hubei Province Key Project of Science and Technology [2006AA201B24]
- Wuhan City Key Project of Industrialization [200720112026]
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Glucocorticoid (GC) are stress hormones, whose cytotoxicity has been shown in various cells. The imbalance of calcium homeostasis is believed to be associated with the dexamethasone (DEX, a synthetic GC)-induced apoptosis. Here we show that in C2C12 myoblasts, DEX markedly up-regulated the expression of inositol 1,4,5-triphosphate receptor 1 (IP3R1) and down-regulated the expression of SERCA1 (sarcoendoplasmic reticulum Ca2+-ATPase 1), leading to calcium overload. Furthermore, the imbalance of calcium homeostasis increased the level of BAX, decreased the level of Bcl-2, induced cytochrome c release and activated caspase-3, leading to intranucleosomal DNA fragmentation and plasma membrane damage, eventually resulting in cell apoptosis. Taken together, by using C2C12 myoblasts as a model system, we demonstrated a novel mechanism for stress hormone-induced apoptosis: it is dependent on the induction of intracellular calcium overload via the alterations of IP3R1 and SERCA1 expressions. (C) 2009 Elsevier Inc. All rights reserved.
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