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Article: Activation of Akt (PKB) and suppression of FKHRL1 in mouse and rat oocytes by stem cell factor during follicular activation and development

TitleActivation of Akt (PKB) and suppression of FKHRL1 in mouse and rat oocytes by stem cell factor during follicular activation and development
Authors
KeywordsMammalian oocytes
Kit
Stem cell factor (SCF)
FKHRL1
Akt
PI3 kinase
Issue Date2005
Citation
Developmental Biology, 2005, v. 281, n. 2, p. 160-170 How to Cite?
AbstractAlthough communications between mammalian oocytes and their surrounding granulosa cells mediated by the Kit-Kit ligand (KL, or stem cell factor, SCF) system have been proven to be crucial for follicular development, Kit downstream signaling pathways in mammalian oocytes are largely unknown. In this study, by using ovaries and isolated oocytes from postnatal mice and rats, we demonstrated for the first time that components of the PI3 kinase pathway, the serine/threonine kinase Akt (PKB) which enhances cellular proliferation and survival, and an Akt substrate FKHRL1 which is a transcription factor that leads to apoptosis and cell cycle arrest, are expressed in mammalian oocytes. By using an in vitro oocytes culture system, we found that oocytes-derived Akt and FKHRL1 are regulated by SCF. Treatment of cultured oocytes with SCF cannot only rapidly phosphorylate and activate Akt, but also simultaneously phosphorylate and may therefore functionally suppress FKHRL1, through the action of PI3 kinase. Together with our in situ hybridization and immunohistochemistry data that Akt and FKHRL1 are mostly expressed in oocytes in primordial and primary ovaries and reports that FKHRL1 gene-deficient mice exhibited excessive activation from primordial to primary follicles as well as enlarged oocyte sizes, we suppose that in mammalian oocytes, actions of granulosa cell derived SCF on primordial to primary follicle transition and subsequent follicle development may involve activation of Akt and inhibition of FKHRL1 activities in oocytes. The role of oocyte's Akt may be to enhance follicle development and the role of oocyte's FKHRL1 may be to inhibit follicle development. We propose that the cascade from granulosa cell SCF to oocyte Kit-PI3 kinase-Akt-FKHRL1 may play an important role to regulate the growth rate of mammalian oocytes and hypothetically also the oocyte secretion of factors that may regulate the activation and early development of ovarian follicles. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/265761
ISSN
2017 Impact Factor: 3.262
2015 SCImago Journal Rankings: 2.554
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorReddy, Pradeep-
dc.contributor.authorShen, Lijun-
dc.contributor.authorRen, Chong-
dc.contributor.authorBoman, Karin-
dc.contributor.authorLundin, Eva-
dc.contributor.authorOttander, Ulrika-
dc.contributor.authorLindgren, Peter-
dc.contributor.authorLiu, Yi Xun-
dc.contributor.authorSun, Qing Yuan-
dc.contributor.authorLiu, Kui-
dc.date.accessioned2018-12-03T01:21:37Z-
dc.date.available2018-12-03T01:21:37Z-
dc.date.issued2005-
dc.identifier.citationDevelopmental Biology, 2005, v. 281, n. 2, p. 160-170-
dc.identifier.issn0012-1606-
dc.identifier.urihttp://hdl.handle.net/10722/265761-
dc.description.abstractAlthough communications between mammalian oocytes and their surrounding granulosa cells mediated by the Kit-Kit ligand (KL, or stem cell factor, SCF) system have been proven to be crucial for follicular development, Kit downstream signaling pathways in mammalian oocytes are largely unknown. In this study, by using ovaries and isolated oocytes from postnatal mice and rats, we demonstrated for the first time that components of the PI3 kinase pathway, the serine/threonine kinase Akt (PKB) which enhances cellular proliferation and survival, and an Akt substrate FKHRL1 which is a transcription factor that leads to apoptosis and cell cycle arrest, are expressed in mammalian oocytes. By using an in vitro oocytes culture system, we found that oocytes-derived Akt and FKHRL1 are regulated by SCF. Treatment of cultured oocytes with SCF cannot only rapidly phosphorylate and activate Akt, but also simultaneously phosphorylate and may therefore functionally suppress FKHRL1, through the action of PI3 kinase. Together with our in situ hybridization and immunohistochemistry data that Akt and FKHRL1 are mostly expressed in oocytes in primordial and primary ovaries and reports that FKHRL1 gene-deficient mice exhibited excessive activation from primordial to primary follicles as well as enlarged oocyte sizes, we suppose that in mammalian oocytes, actions of granulosa cell derived SCF on primordial to primary follicle transition and subsequent follicle development may involve activation of Akt and inhibition of FKHRL1 activities in oocytes. The role of oocyte's Akt may be to enhance follicle development and the role of oocyte's FKHRL1 may be to inhibit follicle development. We propose that the cascade from granulosa cell SCF to oocyte Kit-PI3 kinase-Akt-FKHRL1 may play an important role to regulate the growth rate of mammalian oocytes and hypothetically also the oocyte secretion of factors that may regulate the activation and early development of ovarian follicles. © 2005 Elsevier Inc. All rights reserved.-
dc.languageeng-
dc.relation.ispartofDevelopmental Biology-
dc.subjectMammalian oocytes-
dc.subjectKit-
dc.subjectStem cell factor (SCF)-
dc.subjectFKHRL1-
dc.subjectAkt-
dc.subjectPI3 kinase-
dc.titleActivation of Akt (PKB) and suppression of FKHRL1 in mouse and rat oocytes by stem cell factor during follicular activation and development-
dc.typeArticle-
dc.description.natureLink_to_OA_fulltext-
dc.identifier.doi10.1016/j.ydbio.2005.02.013-
dc.identifier.pmid15893970-
dc.identifier.scopuseid_2-s2.0-21144445994-
dc.identifier.volume281-
dc.identifier.issue2-
dc.identifier.spage160-
dc.identifier.epage170-
dc.identifier.isiWOS:000229311600002-

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