The resumption of oocyte meiosis is a critical step for the progression of oocyte development, which requires an intimate collaboration of a variety of hormones and growth factors. Insulin-like growth factor I (IGF-I) and epidermal growth factor (EGF) family are well recognized to promote oocyte maturation. However, the mechanism by which they coordinate this process remains unknown. The present study demonstrated that IGF-I can increase egfr mRNA and protein levels in follicle cell culture or intact follicles. This stimulation can be significantly inhibited by IGF-IR specific inhibitor, NVP-ADW742. The inhibitors against phosphatidylinositol-3-kinase (PI3K), phosphoinositide-dependent protein kinase 1 (PDK1) and Akt also dramatically abolished IGF-I-induced egfr expression, suggesting that the classical PI3K/Akt pathway mediated the action of IGF-I in this regulation. We further found that not only was the protein level of Egfr increased, but also the phosphorylation level was enhanced by IGF-I. Unlike egfr, IGF-I failed to stimulate the expression of Egf-like ligands whereas decreased the level of protein-tyrosine phosphatase, receptor type, kappa (ptprk), a protein tyrosine phosphatase. The oocyte maturation assay further confirmed that IGF-I initiates this regulation through its cognate receptor in the follicle cells. Taken together, IGF-I promoted oocyte maturation, in part at least, through Egf-like ligands/Egfr pathway. This study sheds light on the cross-talk between two important growth factors in the zebrafish ovary and the mechanism underlying the IGF-I induction on oocyte maturation.
Keywords: Epidermal growth factor; Folliculogenesis; Insulin-like growth factor; Oocyte maturation; Ovary.
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