‘Free’ inhibin α subunit is expressed by bovine ovarian theca cells and its knockdown suppresses androgen production

Laird, M., Glister, C., Cheewasopit, W., Satchell, L. S., Bicknell, A. B. and Knight, P. G. ORCID: https://orcid.org/0000-0003-0300-1554 (2019) ‘Free’ inhibin α subunit is expressed by bovine ovarian theca cells and its knockdown suppresses androgen production. Scientific Reports, 9. 19793. ISSN 2045-2322 doi: 10.1038/s41598-019-55829-w

Abstract/Summary

Inhibins are ovarian dimeric glycoprotein hormones that suppress pituitary FSH production. They are synthesised by follicular granulosa cells as α plus βA/βB subunits (encoded by INHA, INHBA, INHBB, respectively). Inhibin concentrations are high in follicular fluid (FF) which is also abundant in ‘free’ α subunit, presumed to be of granulosal origin, but its role(s) remains obscure. Here, we report the unexpected finding that bovine theca cells show abundant INHA expression and ‘free’ inhibin α production. Thus, theca cells may contribute significantly to the inhibin α content of FF and peripheral blood. In vitro, knockdown of thecal INHA inhibited INSL3 and CYP17A1 expression and androgen production while INSL3 knockdown reduced INHA and inhibin α secretion. These findings suggest a positive role of thecal inhibin α on androgen production. However, exogenous inhibin α did not raise androgen production. We hypothesised that inhibin α may modulate the opposing effects of BMP and inhibin on androgen production. However, this was not supported experimentally. Furthermore, neither circulating nor intrafollicular androgen concentrations differed between control and inhibin α-immunized heifers, casting further doubt on thecal inhibin α subunit having a significant role in modulating androgen production. Role(s), if any, played by thecal inhibin α remain elusive.

Item Type	Article
URI	https://reading-clone.eprints-hosting.org/id/eprint/88008
Identification Number/DOI	10.1038/s41598-019-55829-w
Refereed	Yes
Divisions	Life Sciences > School of Biological Sciences > Biomedical Sciences
Publisher	Nature Publishing Group
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