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Cyclooxygenase-2 and Prostaglandin E₂(PGE₂) Receptor Messenger RNAs Are Affected by Bovine Oocyte Maturation Time and Cumulus-Oocyte Complex Quality, and PGE₂ Induces Moderate Expansion of the Bovine Cumulus In Vitro¹

^a Departments of Obstetrics and Gynaecology and ^b Physiology, The University of Western Ontario, London, Ontario, Canada N6A 5C1 ^c Department of Veterinary Physiology and Pharmacology, College of Veterinary Medicine, Texas A&M University, College Station, Texas 77843-4466

ABSTRACT

Expression of cyclooxygenase-2 (COX-2) and prostaglandin E₂ (PGE₂) receptor 2 (EP2) are necessary for rodent cumulus expansion in vivo. Prostaglandin E₂ receptor 3 (EP3) has been detected in bovine preovulatory follicles and corpora lutea. The current experiments examined the effect of PGE₂ on bovine cumulus expansion in vitro and expression of COX-2, EP1, EP2, EP3, and EP4 mRNAs in bovine cumulus-oocyte complexes (COCs) at 0, 6, 12, 18, and 24 h time points during maturation in vitro. Concentrations of PGE₂ above 50 ng/ml resulted in moderate cumulus expansion of bovine COCs, but expansion did not occur in the absence of serum. COX-2 mRNA expression increased in bovine COCs at 6 h and 12 h of maturation, then decreased. EP2 mRNA was detectable by reverse transcription-polymerase chain reaction at all time points. EP3 mRNA expression increased in COCs from 0 to 6 h and remained at this higher level through the culture period. Very low levels of EP4 mRNA expression were detectable, but EP1 was not detected in bovine COCs. Because EP receptor mRNAs and COX-2 mRNA are expressed in bovine COCs, there exists the potential for a prostaglandin autocrine/paracrine regulatory pathway during oocyte maturation. Differential expression of the EP3 mRNA among varying COC classes indicates that this gene product may be a useful marker of oocyte competence. Although the PGE₂ pathway is involved in cumulus expansion, serum factors are required to mediate PGE₂-induced expansion.

FOOTNOTES

First decision: 8 January 2001.

¹ This work was supported by the National Institute of Child Health and Human Development, National Cooperative Program on Non-Human In Vitro Fertilization and Embryo Development, USA. M.D.C. was supported by a Payton-Collins Women's Health postdoctoral fellowship.

² Correspondence: Michele D. Calder, Departments of Obstetrics and Gynaecology and Physiology, Rm. 238 Medical Sciences Bldg., The University of Western Ontario, London, ON, Canada N6A 5C1. FAX: 519 661 3827; michele.calder{at}med.uwo.ca

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