Culture conditions profoundly impact phenotype in BEAS-2B, a human pulmonary epithelial model

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14 Scopus citations

Abstract

BEAS-2B, an immortalized, human lung epithelial cell line, has been used to model pulmonary epithelial function for over 30years. The BEAS-2B phenotype can be modulated by culture conditions that include the presence or absence of fetal bovine serum (FBS). The popularity of BEAS-2B as a model of arsenic toxicology, and the common use of BEAS-2B cultured both with and without FBS, led us to investigate the impact of FBS on BEAS-2B in the context of arsenic toxicology. Comparison of genome-wide gene expression in BEAS-2B cultured with or without FBS revealed altered expression in several biological pathways, including those related to carcinogenesis and energy metabolism. Real-time measurements of oxygen consumption and glycolysis in BEAS-2B demonstrated that FBS culture conditions were associated with a 1.4-fold increase in total glycolytic capacity, a 1.9-fold increase in basal respiration, a 2.0-fold increase in oxygen consumed for ATP production and a 2.8-fold increase in maximal respiration, compared with BEAS-2B cultured without FBS. Comparisons of the transcriptome changes in BEAS-2B resulting from FBS exposure to the transcriptome changes resulting from exposure to 1μM sodium arsenite revealed that mRNA levels of 43% of the arsenite-modulated genes were also modulated by FBS. Cytotoxicity studies revealed that BEAS-2B cells exposed to 5% FBS for 8weeks were almost 5 times more sensitive to arsenite cytotoxicity than non-FBS-exposed BEAS-2B cells. Phenotype changes induced in BEAS-2B by FBS suggest that culture conditions should be carefully considered when using BEAS-2B as an experimental model of arsenic toxicity.

Original languageEnglish (US)
Pages (from-to)945-951
Number of pages7
JournalJournal of Applied Toxicology
Volume35
Issue number8
DOIs
StatePublished - Aug 1 2015

Keywords

  • Arsenic
  • BEAS-2B
  • Energy metabolism
  • FBS
  • Gene expression
  • Glycolysis

ASJC Scopus subject areas

  • Toxicology

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