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.

Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells

dc.contributor.author	Togher, Katie L.
dc.contributor.author	Kenny, Louise C.
dc.contributor.author	O'Keeffe, Gerard W.
dc.contributor.funder	Science Foundation Ireland	en
dc.contributor.funder	University College Cork	en
dc.contributor.funder	College of Medicine and Health, University College Cork
dc.date.accessioned	2018-01-30T10:21:33Z
dc.date.available	2018-01-30T10:21:33Z
dc.date.issued	2017-02-21
dc.date.updated	2018-01-30T09:52:48Z
dc.description.abstract	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.	en
dc.description.sponsorship	College of Medicine and Health, University College Cork (Translational Research Access Program (TRAP) Award)	en
dc.description.status	Peer reviewed	en
dc.description.version	Published Version	en
dc.format.mimetype	application/pdf	en
dc.identifier.citation	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	en
dc.identifier.doi	10.1155/2017/6169310
dc.identifier.endpage	10	en
dc.identifier.issn	1687-8876
dc.identifier.issn	1687-8884
dc.identifier.journaltitle	International Journal of Cell Biology	en
dc.identifier.startpage	1	en
dc.identifier.uri	https://hdl.handle.net/10468/5342
dc.identifier.volume	2017	en
dc.language.iso	en	en
dc.publisher	Hindawi Publishing Corporation	en
dc.relation.project	info:eu-repo/grantAgreement/SFI/SFI Research Centres/12/RC/2272/IE/Irish Centre for Fetal and Neonatal Translational Research (INFANT)/	en
dc.relation.project	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./	en
dc.rights	© 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.	en
dc.rights.uri	https://creativecommons.org/licenses/by/4.0/	en
dc.subject	Cortisol	en
dc.subject	HDAC	en
dc.title	Class-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cells	en
dc.type	Article (peer-reviewed)	en