论文成果
Fibroblast growth factors and epidermal growth factor cooperate with oocyte-derived members of the TGFbeta superfamily to regulate Spry2 mRNA levels in mouse cumulus cells.
  • 发表刊物:
    Biol Reprod
  • 刊物所在地:
    USA
  • 关键字:
    BMP15, EGF, FGF8, follicular development, GDF9, gene regulation, granulosa cells, oocytes, sprouty 2
  • 摘要:
    Mouse oocytes produce members of the transforming growth factor beta (TGFbeta) superfamily, including bone morphogenetic protein 15 (BMP15) and growth differentiation factor 9 (GDF9), as well as fibroblast growth factors (FGFs). These growth factors cooperate to regulate cumulus cell function. To identify potential mechanisms involved in these interactions, the ability of fully grown oocytes to regulate expression of BMP or FGF antagonists in cumulus cells was examined. Oocytes promoted cumulus cell expression of transcripts encoding antagonists to TGFbeta superfamily members, including Grem2, Htra1, Htra3, and Nog mRNAs. In contrast, oocytes suppressed cumulus cell expression of Spry2 mRNA, which encodes a regulator of receptor tyrosine kinase signals, such as FGF and epidermal growth factor (EGF) receptor signals. The regulation of Spry2 mRNA levels in cumulus cells was studied further as a model for analysis of potential mechanisms for cooperativity of FGF/EGF signaling with oocyte-derived members of the TGFbeta superfamily. Oocytes suppressed basal and FGF-stimulated Spry2 mRNA levels in cumulus cells but promoted EGF-stimulated levels. Furthermore, recombinant TGFbeta superfamily proteins, including BMP15 and GDF9, mimicked these effects of oocytes. Elevated expression of Spry2 mRNA in cumulus and mural granulosa cells correlated with human chorionic gonadotropin-induced expression of mRNAs encoding EGF-like peptides. Therefore, oocyte-derived members of the TGFbeta superfamily suppress FGF-stimulated Spry2 mRNA levels before the luteinizing hormone surge but promote Spry2 mRNA levels stimulated by EGF receptor-mediated signals after the surge.
  • 全部作者:
    You-Qiang Su, Qinglei Li, Karen Wigglesworth, Martin M Matzuk
  • 第一作者:
    Koji Sugiura
  • 论文类型:
    Research Articles
  • 通讯作者:
    John J Eppig
  • 论文编号:
    10.1095/biolreprod.109.078485
  • 卷号:
    81
  • 期号:
    5
  • 页面范围:
    833-841
  • ISSN号:
    0006-3363
  • 是否译文:
  • 发表时间:
    2009-11-01

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