Retinoic acid and retinaldehyde dehydrogenase are not involved in the specific induction of the follicle-stimulating hormone β subunit by trichostatin A, a selective inhibitor of histone deacetylase

The selective histone deacetylase inhibitor, trichostatin A (TSA), increases follicle-stimulating hormone beta subunit (FSH beta) mRNA expression but not alpha- and luteinizing hormone beta (LH beta)-subunits in both the pituitary gonadotrophic cell line L beta T2 and primary cultures of rat anterior pituitary cells. TSA increased histone acetylation in whole cell lysates in both cells. In addition, retinaldehyde dehydrogenases (RALDHs), which are retinoic acid (RA)-synthesizing enzymes, were induced by TSA in these cells. Anacardic acid, a histone acetyltransferase inhibitor that prevents histone acetylation, significantly inhibited TSA-induced FSH beta mRNA expression as well as TSA-induced RALDH2 and RALDH3 mRNA expression. Similar to the effect of TSA, gonadotropin-releasing hormone stimulated RALDH expression in L beta T2 cells. RA directly applied to the pituitary cells stimulated the transcriptional activity of the FSH beta promoter. In addition, alpha- and LH beta-subunit promoters were also activated by RA. Our results suggest that TSA specifically increases FsH beta expression with a concomitant increase in RALDHs; however, RALDH and RA are not directly involved in the specific regulation of FSH beta by TSA. (C) 2015 Elsevier Inc. All rights reserved.