Abstract
Investigating cell death signaling using cell culture is commonly performed to examine the effects of novel pharmaceuticals or to further characterize discrete cellular signaling pathways. Here, we provide data regarding the cell death response to either cisplatin or A23187 in sub-confluent C2C12 cells, by utilizing several concentrations and incubation times for each chemical. These data include an assessment of the activation of the proteolytic enzymes caspase-3, caspase-8, caspase-9, calpain, and cathepsin B/L. Additionally, the expression of the apoptosis-regulating proteins Bax, Bcl2, and p53 are presented.
Highlights
Investigating cell death signaling using cell culture is commonly performed to examine the effects of novel pharmaceuticals or to further characterize discrete cellular signaling pathways
Provides data regarding the specific pathways of cell death activation in C2C12 cells to either cisplatin or A23187
The data demonstrate that cell death in C2C12 cells by cisplatin involves significant activation of p53 and caspases, while A23187 involves caspase-independent mechanisms
Summary
Cells were administered cisplatin or A23187 and collected at several time points. They were prepared for spectrofluorometric assessment of proteolytic enzyme activity or were analyzed for apoptosis-related protein expression using immunoblotting. The data describe the cell death response in proliferating C2C12 cells following exposure to several concentrations and incubation periods with either cisplatin or A23187. Provides data regarding the specific pathways of cell death activation in C2C12 cells to either cisplatin or A23187. The data demonstrate that cell death in C2C12 cells by cisplatin involves significant activation of p53 and caspases, while A23187 involves caspase-independent mechanisms. Despite the common use of cisplatin (CisPL) and Ca2 þ ionophores such as A23187 to induce apoptosis in cell culture experiments, limited evidence exists in C2C12 cells. We present data describing the cell death response in sub-confluent C2C12 cells exposed to CisPL or A23187 (Fig. 1)
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