What growth factors are involved in the pathogenesis of gonadotroph adenomas is not yet known. Activin is one possible candidate because it stimulates growth and differentiation in many cells, including the gonadotroph cell, and it stimulates FSH secretion, characteristic of gonadotroph adenomas. As activin beta B-subunit is expressed in gonadotroph adenomas, we sought to determine whether activin receptor II and follistatin are also expressed. Total ribonucleic acid (RNA) was extracted from 10 gonadotroph adenomas that did not express pit-1 and was reverse transcribed. The resulting complementary DNAs for human activin receptor II and follistatin were amplified by PCR. All 10 adenomas expressed activin receptor II messenger RNA (mRNA), as did nonadenomatous pituitary tissue. Only 2 of the 10 gonadotroph adenomas expressed detectable follistatin mRNA, although all 4 nonadenomatous pituitaries did. Quantitation of follistatin mRNA by competitive reverse transcription-PCR showed that none of the 10 gonadotroph adenomas expressed as much follistatin mRNA as did the 4 nonadenomatous pituitaries, and 8 of the 10 expressed less than 10% as much. Immunospecific staining showed follistatin in the cytoplasm of the gonadotroph cells of all 5 nonadenomatous pituitaries studied, but only faintly in 1 gonadotroph adenoma and not at all in the other 9. These results suggest that pit-1-negative gonadotroph adenomas express less follistatin mRNA and follistatin peptide than do nonadenomatous gonadotroph cells. A consequence could be less binding, and thereby enhanced effectiveness, of activin, contributing to adenoma growth.
As an initial step in determining whether activin could play a role in the development of gonadotroph adenomas, we attempted to determine if activin/inhibin subunit messenger ribonucleic acids (mRNAs) are expressed by these pituitary tumors. We selected 19 pituitary adenomas that had been excised by transsphenoidal surgery and determined by immunocytochemical criteria to be gonadotroph adenomas. Total RNA was extracted from these adenomas and reverse transcribed. The resulting pit-1 complementary DNA, expected to be present only in somatotroph, lactotroph, and thyrotroph cells, was amplified by the polymerase chain reaction to test the possibility that the adenoma tissue was contaminated by normal pituitary tissue. Only the 10 adenomas that did not express pit-1 mRNA were subjected to further analysis by polymerase chain reaction amplification of the adenoma reverse transcriptase products for the activin/inhibin beta B-, beta A-. and alpha-subunits. All 10 adenomas expressed beta B-subunit, none of the 10 expressed the beta A-subunit, and 6 of the 10 expressed the alpha-subunit. We conclude that gonadotroph adenomas express mRNAs for activin/inhibin beta B- and alpha-subunits. The relationship of beta B expression to the pathogenesis of gonadotroph adenomas remains to be determined.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.