Activin subunit, follistatin, and activin receptor gene expression in the prepubertal female rat pituitary.
In the prepubertal female rat, a transient and selective increase in FSH secretion and mRNA expression by the pituitary gland occurs toward the end of the second postnatal week of life. To begin to investigate the possibility that activin may play a role in up-regulating FSH during this time, we have studied the ontogeny of the expression of the activin ss subunits, follistatin, and activin receptor subtypes in the prepubertal female rat pituitary. The levels of expression of ssA, ssB, and follistatin mRNAs were determined in the pituitary gland on postnatal days (PND) 8, 10, 12, 15, and 21 by semiquantitative reverse transcription-polymerase chain reaction. All values were compared to those of adult females killed on diestrus. mRNA levels of subunit ssA were significantly (p < 0.05) elevated on all postnatal days examined; ssB mRNA levels were elevated above adult levels only on PND 10 (p < 0.05). Follistatin mRNA was high on PND 8 (p < 0.05) and then decreased to adult levels. The level and distribution of activin receptor type II subtype mRNAs were determined by in situ hybridization. Activin receptor type II (Act RII) mRNA expression was diffusely expressed throughout all areas of the pituitary. Activin receptor type IIB (Act RIIB), on the other hand, was highly expressed by a subset of anterior pituitary cells. In situ hybridization for activin receptor subtype mRNAs was combined with immunocytochemistry to detect FSH-containing cells. We determined that in the infantile female pituitary, Act RII mRNA was generally not expressed in FSH-immunoreactive cells, while Act RIIB mRNA was expressed in FSH-immunoreactive cells. Act RII mRNA was lower on PND 10 and 15 when compared to PND 21 (p < 0.05), whereas Act RIIB mRNA expression did not change with age. These data suggest that the essential components of the activin regulatory system are present in the infantile female pituitary gland and thus may be involved in the differential regulation of FSH at this time.
Wilson
M E
ME
Program in Molecular Biology and Department of Cell Biology, Neurobiology, and Anatomy, Loyola University, Stritch School of Medicine, Maywood, Illinois 60153, USA.
Handa
R J
RJ
D029404:Activin Receptors; D028341:Activins; D000818:Animals; D005260:Female; D038681:Follistatin; D018507:Gene Expression Regulation, Developmental / Q000502:physiology*; D006023:Glycoproteins / Q000096:biosynthesis* / Q000235:genetics; D006133:Growth Substances / Q000096:biosynthesis* / Q000235:genetics; D007091:Image Processing, Computer-Assisted; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007265:Inhibins / Q000096:biosynthesis* / Q000235:genetics; D010902:Pituitary Gland / Q000254:growth & development* / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D012333:RNA, Messenger / Q000096:biosynthesis; D051381:Rats; D017978:Receptors, Growth Factor / Q000096:biosynthesis* / Q000235:genetics
D038681:Follistatin; D006023:Glycoproteins; D006133:Growth Substances; D012333:RNA, Messenger; D017978:Receptors, Growth Factor; D028341:Activins; D007265:Inhibins; D029404:Activin Receptors