Regulation of follicle-stimulating hormone-receptor messenger RNA in hen granulosa cells relative to follicle selection.
Both the viability of hen prehierarchal follicles and subsequent differentiation associated with the selection of a single follicle per day into the preovulatory hierarchy depend on circulating FSH and the expression of FSH receptor (FSH-R) in granulosa cells. The present study addresses mechanisms that mediate both basal expression plus selective up-regulation of FSH-R mRNA in granulosa cells from prehierarchal follicles. Results demonstrate that FSH-R mRNA is both expressed and functional in granulosa cells collected from growing prehierarchal follicles as small as those of 1-2 mm in diameter, as indicated by rapid induction of steroidogenic acute regulatory (StAR) protein expression by FSH in vitro. Real-time polymerase chain reaction determined that relative FSH-R expression within the granulosa layer from individual prehierarchal follicles of 6-8 mm in diameter was similar among the 8-13 follicles within this cohort, with the notable exception that the granulosa layer from a single follicle (presumably the selected follicle) showed elevated expression. Levels of FSH-R mRNA expression were enhanced by both recombinant human (rh) transforming growth factor (TGF) beta1 and, to a lesser extent, rh-activin A after 20 h of culture. This stimulatory effect was effectively blocked by mitogen-activated protein (MAP) kinase signaling induced by TGF alpha treatment. Finally, inhibition of MAP kinase signaling, using the selective inhibitor U0126, promoted FSH-R expression and further enhanced TGF beta1-induced FSH-R expression in vitro. Collectively, results suggest that premature granulosa cell differentiation normally is suppressed by tonic MAP kinase signaling. At the time of follicle selection, a release from inhibitory MAP kinase signaling is proposed to occur, which enables the full potentiation of FSH-R expression mediated by intrafollicular factors.
Woods
Dori C
DC
Department of Biological Sciences, The University of Notre Dame, Notre Dame, Indiana 46556, USA.
Johnson
A L
AL
D028341:Activins / Q000502:physiology; D000818:Animals; D002645:Chickens; D003338:Corpus Luteum / Q000254:growth & development* / Q000378:metabolism; D005260:Female; D006107:Granulosa Cells / Q000378:metabolism*; D006801:Humans; D028322:Inhibin-beta Subunits / Q000502:physiology; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D023421:Models, Animal; D010060:Ovulation / Q000378:metabolism; D012333:RNA, Messenger / Q000032:analysis / Q000378:metabolism*; D011962:Receptors, FSH / Q000235:genetics / Q000378:metabolism*; D011994:Recombinant Proteins; D016212:Transforming Growth Factor beta / Q000502:physiology; D053773:Transforming Growth Factor beta1; D015854:Up-Regulation
D012333:RNA, Messenger; D011962:Receptors, FSH; D011994:Recombinant Proteins; C508960:TGFB1 protein, human; D016212:Transforming Growth Factor beta; D053773:Transforming Growth Factor beta1; C422405:activin A; D028341:Activins; D028322:Inhibin-beta Subunits; D020928:Mitogen-Activated Protein Kinases