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Exogenous progesterone given early in the ovine estrous cycle results in precocious luteolysis. It has been suggested that under this circumstance regression of the corpus luteum is caused by an advancement in the timing of uterine secretion of prostaglandin F2 alpha. Uterine tissues were obtained from ewes following administration of progesterone (or injection vehicle), fixed in paraformaldehyde, and embedded in paraffin. Tissue sections were hybridized using an 35S-labeled cRNA probe specific for cyclooxygenase mRNA. There was approximately an eight-fold increase in the level of hybridization signal, localized mainly to uterine glands, consequential to treatment with progesterone. Thus, progesterone appears to control expression of the endometrial gene and(or) the stability of the message encoding for a rate-limiting enzyme involved in metabolism of arachidonic acid to its luteolytic product, thereby resolving the length of the nonpregnant cycle.
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