earticle

영어

Previously, the expression of caspase-3 siRNA could not effectively inhibit sodium butyrate (NaBu)-induced apoptotic cell death of recombinant Chinese Hamster ovary (rCHO) cells producing human thrombopoietin (hTPO)2). Caspase-3 siRNA expressing cells appeared to compensate for the lack of caspase-3 by increasing active caspase-7 levels. For the successful inhibition of NaBu-induced apoptosis of rCHO cells, both caspase-3/7 were down-regulated
using the siRNA expression vector system. Co-down-regulation of caspase-3/7 increased cell viability and extended culture longevity in serum-free culture in the presence or absence of 1 mM NaBu addition. In the cultures with 1 mM NaBu addition, the maximum hTPO concentration in caspase-3/7 down-regulated rCHO cells was approximately 55% higher than that in rCHO cells without down-regulation of caspases and approximately 16% higher than caspase-3
down-regulated rCHO cells. However, in the culture with 3 mM NaBu, this strategy could not dramatically enhance the culture longevity and hTPO production, compared to Bcl-2 overexpression1). The different result in hTPO production may be because the down-regulation of caspase-3/7, unlike Bcl-2 overexpression, could not maintain mitochondrial membrane potential in the presence of 3 mM NaBu.