Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells
Supplementary Figure 1
Togher, Katie L.
Kenny, Louise C.
O'Keeffe, Gerard W.
Hindawi Publishing Corporation
Exposure to maternal cortisol plays a crucial role in fetal organogenesis. However, fetal overexposure to cortisol has been linked to a range of short- and long-term adverse outcomes. Normally, this is prevented by the expression of an enzyme in the placenta called 11-beta hydroxysteroid dehydrogenase type 2 (11β-HSD2) which converts active cortisol to its inactive metabolite cortisone. Placental 11β-HSD2 is known to be reduced in a number of adverse pregnancy complications, possibly through an epigenetic mechanism. As a result, a number of pan-HDAC inhibitors have been examined for their ability to promote 11β-HSD2 expression. However, it is not known if the effects of pan-HDAC inhibition are a general phenomenon or if the effects are dependent upon a specific class of HDACs. Here, we examined the ability of pan- and class-specific HDAC inhibitors to regulate 11β-HSD2 expression in JEG3 cells. We find that pan-, class I, or class IIa HDAC inhibition promoted 11β-HSD2 expression and prevented cortisol or interleukin-1β-induced decrease in its expression. These results demonstrate that targeting a specific class of HDACs can promote 11β-HSD2 expression in JEG3 cells. This adds to the growing body of evidence suggesting that HDACs may be crucial in maintaining normal fetal development.
Cortisol , HDAC
Togher, K. L., Kenny, L. C. and O'Keeffe, G. W. (2017) 'Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells', International Journal of Cell Biology, 6169310 (10 pp). doi:10.1155/2017/6169310