The Expression Pattern of the c-kit Ligand in Gonads of Mice Supports a Role for the c-kit Receptor in Oocyte Growth and in Proliferation of Spermatogonia

Transforming growth factor-β regulates Kit ligand expression in rat ovarian surface epithelial cells

“…Although Kit expression can be upregulated by activation of this pathway in some cell types (Nishina et al, 1992;Ogawa et al, 1995), Kit was not expressed in ROSE 199 cells treated with dbcAMP. In contrast, dbcAMP increased the expression of KL mRNA which is in agreement with its e ects on KL expression in granulosa cells (Manova et al, 1993) and Sertoli cells (Rossi et al, 1991). Coincident with the enhanced expression of KL, dbcAMP also strongly inhibited ROSE 199 cell proliferation; however the lack of Kit receptors in these cells would suggest that the altered gene expression was not responsible for the changes in proliferation.…”

“…Rat OSE cells in culture had clear cytoplasm, well-de®ned borders and formed con¯uent monolayers, similar to those described by Adams and Auersperg (1981). Furthermore, the ovarian cells underlying the OSE cells are stroma cells, which express Kit (Manova et al, 1993;Motro and Bernstein, 1993;Lammie et al, 1994), so the absence of Kit expression in the rat OSE cell preparation would suggest that there was no stromal cell contamination in these cultures.…”

“…This overgrowth ultimately led to the formation of extensive invagination of epithelial tubules into the ovary cortex and, by 13 ± 20 weeks, these animals exhibited complex formations of tubular adenomas composed of invasive epithelial tubules and interstitial cells. Although the mechanism by which stromal-epithelial interactions are disrupted is currently unknown, the evidence that theca cells express Kit receptors (Motro and Bernstein, 1993;Manova et al, 1993) would suggest that theca cell function has been compromised by Kit x/v mutations. The phenotype of the mutant mice would suggest that theca cells normally mediate growth inhibition of OSE cells since loss of normal Kit function results in OSE cell invasion into stroma.…”

Growth and differentiation factor 9 promotes oocyte growth at the primary but not the early secondary stage in three-dimensional follicle culture

“…A potential candidate for such a factor is KIT ligand. Consistent with this model, KIT-ligand expression is limited in the primary follicle [66,68] but significantly higher at the secondary and subsequent stages of folliculogenesis [68]. Further, findings in GDF9 null mice suggested GDF9 might suppress KITligand expression at the primary stage [66], which suggests a potential mechanism for the observed stage-specific effects.…”

Expression of Sox9 in granulosa cells lacking the estrogen receptors, ERα and ERβ

“…Indeed, because both cell types have a common embryologic origin from the genital ridge (reviewed in Swain and LovellBadge, 1999) and are similar with respect to their functions of nurse cells for the germ cells and to their main regulation by the gonadotropin FSH, they express similar sets of genes, e.g., genes encoding AMH (Mü nsterberg and Lovell-Badge, 1991;Hirobe et al, 1992, and references therein), inhibin/activin (Griswold, 1993;Richards, 1994), c-kit ligand (Manova et al, 1993;Richards, 1994;Vincent et al, 1998), aromatase (Richards, 1994;Levallet et al, 1998), and SGP-2 (Ahuja et al, 1994;Aronow et al, 1993). Sox9 is one of the very few genes whose expression profile allows to unambiguously distinguish Sertoli and their precursors from granulosa cells: Sox9 is an early and permanent marker of the Sertoli cell lineage, as it starts to be expressed in the male genital ridge and is subsequently strongly expressed in fetal, postnatal, and adult Sertoli cells (Morais da Silva et al, 1996).…”