PUBLICATION
Insulin-like growth factor I promotes oocyte maturation through increasing the expression and phosphorylation of epidermal growth factor receptor in the zebrafish ovary
- Authors
- Xie, L., Tang, Q., Yang, L., Chen, L.
- ID
- ZDB-PUB-151125-3
- Date
- 2016
- Source
- Molecular and Cellular Endocrinology 419: 198-207 (Journal)
- Registered Authors
- Keywords
- epidermal growth factor, folliculogenesis, insulin-like growth factor, oocyte maturation, ovary
- MeSH Terms
-
- Animals
- Cells, Cultured
- Female
- Gene Expression Regulation
- Oogenesis
- Ovary/cytology*
- Ovary/metabolism
- Phosphorylation
- Receptor-Like Protein Tyrosine Phosphatases, Class 2/genetics
- Receptor-Like Protein Tyrosine Phosphatases, Class 2/metabolism
- Signal Transduction
- Somatomedins/genetics
- Somatomedins/metabolism*
- Zebrafish
- Zebrafish Proteins/genetics
- Zebrafish Proteins/metabolism*
- PubMed
- 26599586 Full text @ Mol. Cell. Endocrinol.
Citation
Xie, L., Tang, Q., Yang, L., Chen, L. (2016) Insulin-like growth factor I promotes oocyte maturation through increasing the expression and phosphorylation of epidermal growth factor receptor in the zebrafish ovary. Molecular and Cellular Endocrinology. 419:198-207.
Abstract
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.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping