Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells
|Togher, Katie L.
|Kenny, Louise C.
|O'Keeffe, Gerard W.
|Science Foundation Ireland
|University College Cork
|College of Medicine and Health, University College Cork
|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.
|College of Medicine and Health, University College Cork (Translational Research Access Program (TRAP) Award)
|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
|International Journal of Cell Biology
|Hindawi Publishing Corporation
|info:eu-repo/grantAgreement/SFI/SFI Research Centres/12/RC/2272/IE/Irish Centre for Fetal and Neonatal Translational Research (INFANT)/
|info:eu-repo/grantAgreement/SFI/SFI Research Frontiers Programme (RFP)/10/RFP/NES2786/IE/Defining the potential of the transmembrane GITR receptor as a novel therapeutic for PNS neuropathies./
|© 2017 Katie L. Togher et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
|Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells
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