## Abstract Undefined follicular factors that may influence nuclear maturation and/or cytoplasmic maturation are required during in vitro maturation of pig oocytes. Epidermal growth factor (EGF), insulin‐like growth factor‐I (IGF‐I), and dialysed porcine follicular fluid (dpFF) were evaluated for t
Mechanism of action of epidermal growth factor-induced porcine oocyte maturation
✍ Scribed by Serdar Coskun; Young C. Lin
- Publisher
- John Wiley and Sons
- Year
- 1995
- Tongue
- English
- Weight
- 766 KB
- Volume
- 42
- Category
- Article
- ISSN
- 1040-452X
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✦ Synopsis
Abstract
EGF has been reported to promote oocyte maturation in several species, although the mechanism of action is not yet known. The present study is designed to determine the pathway used by EGF to enhance porcine oocyte maturation. Oocytes were aspirated from 2–5 mm follicles and cultured with various treatments in Medium‐199 at 37°C, 100% relative humidity, and 5% CO~2~ for 48 hr for the maturation study and 3 hr for intracellular cAMP measurement. Although treatment with 100 IU/ml hCG stimulated both intracellular cAMP formation and oocyte maturation, 10 ng/ml EGF stimulated oocyte maturation only. Dibutyryl cAMP (dbcAMP) inhibited oocyte maturation at 10^−5^, 10^−4^, and 10^−3^ M concentrations in the control medium. However, in the presence of 10 ng/ml EGF, dbcAMP inhibited oocyte maturation only at a concentration of 10^−3^ M. Increasing concentrations of EGF (i.e., 25 and 50 ng/ml) were ineffective in overcoming the inhibitory effect of dbcAMP at 10^−3^ M. In contrast, EGF reversed the decreased maturation rate caused by transforming growth factor‐β. Phorbol myristate acetate (PMA), a tumor‐promoting phorbol ester, enhanced the spontaneous maturation rate; 4α‐phorbol dideconoate, an inactive phorbol ester, did not show this effect. PMA‐ and EGF‐stimulated porcine oocyte maturation is reversed by calphostin‐C, a PKC inhibitor. In conclusion, EGF's promotional activity on porcine oocyte maturation is independent of the cAMP pathway and probably mediated by the PKC pathway. © 1995 wiley‐Liss, Inc.
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