Journal
PROCESS BIOCHEMISTRY
Volume 46, Issue 11, Pages 2201-2204Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.procbio.2011.07.017
Keywords
Dimethyl sulfoxide; Bcl-xL; Apoptosis; rCHO cells; Inducible expression
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Funding
- KRIBB
- Korean Government [351-2009-2-D00054]
- National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2009-0082336]
- National Research Foundation of Korea [351-2009-2-D00054] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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Dimethyl sulfoxide (DMSO) can increase the specific productivity (q) of foreign proteins in mammalian cells, while it can also induce cell death, particularly apoptosis. Bcl-xL is a typical anti-apoptotic protein that inhibits the apoptosis in recombinant Chinese hamster ovary (rCHO) cell culture. To evaluate the potential role of Bcl-xL overexpression on DMSO-mediated erythropoietin (EPO) production, we used EPO-producing rCHO cells with regulated Bcl-xL overexpression (EPO-off-Bcl-xL) by doxycycline. Although DMSO addition enhanced specific EPO productivity (q(Epo)), it also induced cell death in EPO-off-Bcl-xL cells. Bcl-xL overexpression reduced the DMSO-induced cell death followed by release of various enzymes from plasma membrane-damaged cells as evidenced from LDH assay, resulting in delayed loss of EPO. However, it did not significantly improve the maximum EPO production. In addition, Bcl-xL overexpression suppressed DMSO-induced apoptosis, characterized by DNA fragmentation and Annexin V staining. Taken together, Bcl-xL overexpression could inhibit DMSO-induced apoptosis, thereby delaying the loss of EPO. (C) 2011 Elsevier Ltd. All rights reserved.
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