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

dc.contributor.authorTogher, Katie L.
dc.contributor.authorKenny, Louise C.
dc.contributor.authorO'Keeffe, Gerard W.
dc.contributor.funderScience Foundation Irelanden
dc.contributor.funderUniversity College Corken
dc.contributor.funderCollege of Medicine and Health, University College Cork
dc.date.accessioned2018-01-30T10:21:33Z
dc.date.available2018-01-30T10:21:33Z
dc.date.issued2017-02-21
dc.date.updated2018-01-30T09:52:48Z
dc.description.abstractExposure 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.sponsorshipCollege of Medicine and Health, University College Cork (Translational Research Access Program (TRAP) Award)en
dc.description.statusPeer revieweden
dc.description.versionPublished Versionen
dc.format.mimetypeapplication/pdfen
dc.identifier.citationTogher, 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:10.1155/2017/6169310en
dc.identifier.doi10.1155/2017/6169310
dc.identifier.endpage10en
dc.identifier.issn1687-8876
dc.identifier.issn1687-8884
dc.identifier.journaltitleInternational Journal of Cell Biologyen
dc.identifier.startpage1en
dc.identifier.urihttps://hdl.handle.net/10468/5342
dc.identifier.volume2017en
dc.language.isoenen
dc.publisherHindawi Publishing Corporationen
dc.relation.projectinfo:eu-repo/grantAgreement/SFI/SFI Research Centres/12/RC/2272/IE/Irish Centre for Fetal and Neonatal Translational Research (INFANT)/en
dc.relation.projectinfo: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.urihttps://creativecommons.org/licenses/by/4.0/en
dc.subjectCortisolen
dc.subjectHDACen
dc.titleClass-specific histone deacetylase inhibitors promote 11-beta hydroxysteroid dehydrogenase type 2 expression in JEG-3 cellsen
dc.typeArticle (peer-reviewed)en
Files
Original bundle
Now showing 1 - 2 of 2
Loading...
Thumbnail Image
Name:
6169310.pdf
Size:
4.99 MB
Format:
Adobe Portable Document Format
Description:
Published Version
Loading...
Thumbnail Image
Name:
SupplementaryMaterials.pdf
Size:
205.46 KB
Format:
Adobe Portable Document Format
Description:
Supplementary Figure 1
License bundle
Now showing 1 - 1 of 1
Loading...
Thumbnail Image
Name:
license.txt
Size:
2.71 KB
Format:
Item-specific license agreed upon to submission
Description: