The Expression of c-kit Protein during Oogenesis and Early Embryonic Development1

Horie, Katsuyuki; Takakura, Kenji; Taii, Shunzo; Narimoto, Kazutaka; Noda, Yoichi; Nishikawa, Satomi; Nakayama, Hiroki; Fujita, Jun; Mori, Takahide

doi:10.1095/biolreprod45.4.547

Cited by 143 publications

(92 citation statements)

References 31 publications

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“…These results confirm earlier studies showing expression of c-Kit protein in oocytes and expression of its mRNA in oocytes and preovulatory granulosa cells (Horie et al 1993, Tanikawa et al 1998. Although several studies on mice have shown that c-Kit is confined to theca interna cells (Manova et al 1990, Horie et al 1991, Keshet et al 1991, Motro et al 1991, Motro & Bernstein 1993), we did not locate its expression in these cells in human ovarian biopsy samples. In this respect, our result is different from that reported by Ito et al (2001), who used RT-PCR and showed the presence of c-Kit mRNA in human ovarian theca and stroma cells.…”

Section: Discussionsupporting

confidence: 89%

Kit ligand and c-Kit are expressed during early human ovarian follicular development and their interaction is required for the survival of follicles in long-term culture

Carlsson¹,

Laitinen²,

Scott³

et al. 2006

Reproduction

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I B Carlsson and M P E Laitinen contributed equally to this paper AbstractThe receptor tyrosine c-Kit and its cognate ligand, c-Kit ligand (KL, stem cell factor, SCF), are involved in ovarian follicular development in several animal species. We studied the expression of KL and c-Kit using in situ hybridization and immunohistochemistry in donated human ovarian cortical tissue. The KL transcripts were expressed in granulosa cells of primary follicles, whereas the expression of c-Kit was confined to the oocyte and granulosa cells in primary and secondary follicles. We employed an ovarian organ culture using firstly serum-containing and then serum-free medium to study the effects of KL and an anti-c-Kit antibody, ACK2, on the development and survival of ovarian follicles in vitro. Culture of ovarian cortical slices for 7 days resulted in a 37% increase in the number of primary follicles and a 6% increase in secondary follicles. The proportion of viable follicles decreased in all cultures. The addition of KL (1, 10 and 100 ng/ml) into the culture media did not affect the developmental stages of the follicles or the proportion of atretic follicles. Inclusion of ACK2 (800 ng/ml) in the culture medium significantly increased the proportion of atretic follicles on days 7 (49 vs 28% in control cultures) and 14 (62 vs 38%) of culture. In conclusion, c-Kit and KL are expressed in human ovaries during follicular development. Blocking the c-Kit receptor induces follicular atresia. The KL/c-Kit signaling system is likely to control the survival of human ovarian follicles during early follicular development. Reproduction (2006) 131 641-649Introduction During a woman's reproductive life less than 1% of the follicles present in the human ovary at birth reach the stage of ovulation, while the rest undergo atresia and are lost. Some of the follicles present at birth start to grow during infancy and childhood, but most of them remain in the resting stage until they either degenerate or enter the growth phase during adult life (Adashi 1991, Gougeon 1996. It is likely that the mechanism behind the loss of germ cells is apoptotic cell death (Tilly 1996). Follicle-stimulating hormone (FSH) has been considered to be a key survival factor for follicles from the antral follicular stage onwards (McGee et al. 1998). However, the regulators of early follicular survival are still poorly characterized.The c-Kit ligand (KL, also called stem cell factor, SCF), a ligand for the c-Kit proto-oncogene receptor tyrosine kinase, is a pluripotent growth factor involved in the differentiation and growth of certain stem cell lineages including hematopoietic stem cells, neuroblasts, melanoblasts and primordial germ cells (PGCs) (Galli et al. 1994). The expression of KL has been detected in granulosa cells in mouse ovaries, while c-Kit receptor is confined to the oocytes and theca interna cells (Manova et al. 1990, Horie et al. 1991, Keshet et al. 1991, Motro et al. 1991, Motro & Bernstein 1993. In contrast to mice, c-Kit protein and mRNA have been detected...

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Section: Discussionsupporting

confidence: 89%

Kit ligand and c-Kit are expressed during early human ovarian follicular development and their interaction is required for the survival of follicles in long-term culture

Carlsson¹,

Laitinen²,

Scott³

et al. 2006

Reproduction

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“…Kit transcripts were absent in both primary and immortalized rat OSE cells and, although Kit expression in other ovarian cell types has been shown to be regulated by various factors including cAMP (Nishina et al, 1992;Ogawa et al, 1995) and human chorionic gonadotropin (Horie et al, 1991), it could not be induced in OSE cells by dbcAMP. Although this observation suggests that Kit does not play a direct role in OSE cell activity, it is equally possible that Kit is important, but is expressed in OSE cells only under speci®c conditions which were not duplicated in culture, or that Kit expression cannot be induced in the immortalized cells used in this study.…”

Section: Discussionmentioning

confidence: 88%

“…Although FSH has not been shown to regulate Kit expression, the LH-like hormone hCG decreases Kit expression in both theca cells and oocytes of mouse ovaries (Motro and Bernstein, 1993;Horie et al, 1991). In addition, both FSH and hCGlike hormones increase KL mRNA expression in granulosa cells of mice (Motro and Bernstein, 1993) and rats (Ismail et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

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

1999

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In preparation for ovulation, paracrine communication between the preovulatory follicle and overlying theca/ stromal cells and ovarian surface epithelium (OSE) must take place to facilitate the degradative and apoptotic events associated with ovulation. Kit tyrosine kinase receptors and their ligand, kit ligand (KL) are expressed within ovarian follicles, and ligand-induced receptor activation appears to account for some of the cell ± cell interactions important for oocyte development. We investigated the expression of Kit receptors and KL in OSE cells and the possibility that modulation of their expression could a ect OSE cell activity. KL mRNA and protein were detected in the OSE cell layer of rat ovaries, and primary cultures of rat OSE as well as the immortalized rat OSE cell line, ROSE 199, expressed KL, but not Kit receptors. Both primary and immortalized OSE cells preferentially expressed KL-1, rather than KL-2, transcripts, suggesting that these cells produce predominantly the soluble form of KL. Activation of the cAMP signalling pathway using dibutyryl cAMP decreased proliferation of ROSE 199 cells and elicited a threefold increase in KL expression. TGF-b similarly inhibited ROSE 199 cell proliferation, but strongly inhibited dibutyryl cAMP-induced KL expression, indicating that changes in KL expression were not directly associated with OSE cell proliferation. The expression of mostly soluble KL in the surface epithelium suggests that this cytokine may be acting in a paracrine fashion, perhaps interacting with nearby Kit receptorbearing theca cells.

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“…The essential role of SCF/c-Kit in oocyte growth and follicular development has been a topic of investigation for decades [18,19]. c-Kit is expressed at the surface of mammalian oocytes at all stages of follicular development in postnatal ovaries of mice, rats, and humans [20,21], whereas SCF/KL is produced only by granulosa cells [7,22]. In fact, treatment of in vitro cultured follicles from 8-day-old mice with SCF/ KL significantly increased the growth rate of oocytes [23].…”

Section: Discussionmentioning

confidence: 99%

Stem cell factor/c-Kit signaling in in vitro cultures supports early mouse embryonic development by accelerating proliferation via a mechanism involving Akt-downstream genes

Lim

Eum

Lee

et al. 2010

J Assist Reprod Genet

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Purpose Stem cell factor (SCF)/c-Kit regulates the proliferation and survival of germ cells or stem cells; however, little is known about the role of SCF/c-Kit in preimplantation embryo development. Methods Using exogenous SCF supplementation and c-Kit siRNA injection, we investigated the role and mechanism of SCF/c-Kit in pre-implantation mouse embryos.Results Addition of soluble SCF to the culture medium improved blastocyst formation. c-Kit gene silencing reduced the rate of blastocyst formation and delayed embryonic development. The number of proliferating cells in c-Kit gene-silenced blastocysts decreased, whereas the number of apoptotic cells in blastocysts obtained from both experimental and the control groups was not affected. RT-PCR, immunostaining and western blotting revealed that proliferation-related Akt downstream targets were substantially affected by c-Kit gene silencing. Conclusion SCF/c-Kit signaling through Akt downstream targets is likely involved in mediating the cleavage and proliferation of blastomeres during mouse pre-implantation embryogenesis.

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The Expression of c-kit Protein during Oogenesis and Early Embryonic Development1

Cited by 143 publications

References 31 publications

Kit ligand and c-Kit are expressed during early human ovarian follicular development and their interaction is required for the survival of follicles in long-term culture

Kit ligand and c-Kit are expressed during early human ovarian follicular development and their interaction is required for the survival of follicles in long-term culture

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

Stem cell factor/c-Kit signaling in in vitro cultures supports early mouse embryonic development by accelerating proliferation via a mechanism involving Akt-downstream genes

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