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CREB activity is required for luteinizing hormone‐induced the expression of EGF‐like factors
Author(s) -
Wang Yakun,
Hao Xiaoqiong,
Yang Jing,
Li Jia,
Zhang Meijia
Publication year - 2016
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.22753
Subject(s) - creb , biology , medicine , endocrinology , luteinizing hormone , epidermal growth factor , human chorionic gonadotropin , receptor , transcription factor , hormone , biochemistry , gene
SUMMARY A surge of luteinizing hormone (LH) from the pituitary gland induces the expression of the epidermal growth factor (EGF)‐like factors, which triggers oocyte maturation, cumulus expansion, and ovulation. How LH induces EGF‐like factor expression is unclear. In the present study, a rapid increase of phosphorylated cAMP response element binding protein (CREB) was observed after the activation of LH receptor by human chorionic gonadotropin. Large antral follicles from equine chorionic gonadotropin‐primed mice were cultured in medium with LH to stimulate the expression of EGF‐like factors. CREB phosphorylation was increased in granulosa cells; conversely KG‐501, a CREB functional inhibitor, significantly reduced LH‐induced gene expression of EGF‐like factors, oocyte meiotic resumption, and cumulus cell expansion. Reduction of CREB expression by Creb siRNA also repressed LH‐induced expression of EGF‐like factors in cultured granulosa cells. Inactivation of mitogen‐activated protein kinase (MAPK3/1) by U0126 inhibited LH‐induced CREB phosphorylation and EGF‐like factors gene expression, whereas the activation of LH receptor increased Akt/protein kinase B phosphorylation, which is involved in LH‐induced CREB phosphorylation and the expression of EGF‐like factors. Thus, LH induces MAPK3/1 and Akt activation, both of which are required for the CREB‐promoted expression of EGF‐like factors in granulosa cells. Mol. Reprod. Dev. 83: 1116–1127, 2016. © 2016 Wiley Periodicals, Inc .