The effects of betamethasone (BM) on endothelial nitric oxide synthase (eNOS) expression in adult baboon femoral arterial endothelial cells

Keiko Aida, Qiang Shi, Jian Wang, John L. Vandeberg, Thomas McDonald, Peter Nathanielsz, Xing Li Wang

    Research output: Contribution to journalArticlepeer-review

    9 Scopus citations


    Glucocorticoids have significant effects on endothelium mediated vascular function throughout life. The baboon model has been used extensively to study cellular responses to glucocorticoids at several stages of the lifespan. Endothelial nitric oxide synthase (eNOS) is a major regulator of endothelium dependent arterial vasodilation. We have previously demonstrated that synthetic glucocorticoids down regulate eNOS in the baboon placenta. We have now conducted studies to determine whether glucocorticoids would alter eNOS expression in adult systemic vascular endothelial cells in this important animal model. We explored this potential mechanism in endothelial cells from femoral arteries of adult baboons at necropsy and cultured to the fourth passage. Endothelial cells were treated with 10-100 nM betamethasone for 24 h at 37 °C. Vascular endothelial growth factor (VEGF) was used as a positive control and medium as negative controls. The role of glucocorticoid receptor mediation in betamethasone-induced eNOS changes was investigated with the glucocorticoid receptor antagonist mifepristone. RNA (real-time quantitative RT-PCR) and protein (ELISA) were extracted and measured for eNOS. Expression and subcellular distribution of glucocorticoid receptor were detected with fluorescence labeled antibody microscopy. eNOS mRNA and protein in baboon endothelial cells were downregulated 25% by betamethasone treatment. This effect was attenuated by pre-incubation with mifepristone (P < 0.01). VEGF upregulated eNOS transcription and translation (P < 0.001), medium did not alter eNOS expression. We observed that mifepristone and VEGF increased glucocorticoid receptor cytoplasmic accumulation by fluorescence microscopy. We conclude that betamethasone can downregulate eNOS in cultured baboon endothelial cells via the glucocorticoid receptor pathway.

    Original languageEnglish (US)
    Pages (from-to)219-224
    Number of pages6
    JournalJournal of Steroid Biochemistry and Molecular Biology
    Issue number4-5
    StatePublished - Aug 2004


    • Baboons
    • Endothelial cells
    • Glucocorticoid receptors
    • Glucocorticoids
    • eNOS

    ASJC Scopus subject areas

    • Endocrinology, Diabetes and Metabolism
    • Biochemistry
    • Molecular Medicine
    • Molecular Biology
    • Endocrinology
    • Clinical Biochemistry
    • Cell Biology


    Dive into the research topics of 'The effects of betamethasone (BM) on endothelial nitric oxide synthase (eNOS) expression in adult baboon femoral arterial endothelial cells'. Together they form a unique fingerprint.

    Cite this