Secretion of progesterone and prostaglandins by cells of bovine corpora lutea from three stages of the luteal phase

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Abstract
The secretion of prostaglandins (PGs) by bovine corpora lutea was investigated. Corpora lutea from the early, early-mid and late-mid stages of the luteal phase were dissociated by collagenase treatment and cultured in monolayer in Dulbecco's modified Eagle's medium containing 10% (v/v) fetal calf serum. Treatment with either LH (100 ng/ml) or dibutyryl cyclic AMP (dbcAMP; 1 mmol/l) had no effect on progesterone secretion by early luteal phase cells but stimulated progesterone secretion two- to fourfold by cells from the latter stages. The secretion rates, per μg cell protein, of 6-keto-PGF1α, PGE2 and PGF2α were substantially greater in cells from the early luteal phase than in those from the latter stages, however, all changes in PG secretion in response to treatments were qualitatively similar between cells from the three stages of the luteal phase. The secretion rate of 6-keto-PGF1α was greater than that of PGE2 or PGF2α and was inhibited by treatment with indomethacin (28 μmol/l) but unaltered by treatment with LH, dbcAMP or butyrate (1 mmol/l). Secretion of PGE2 was inhibited by indomethacin but stimulated two-to threefold by treatment with either dbcAMP or butyrate. Secretion of PGF2α was minimal and not inhibited further by treatment with indomethacin, but was stimulated 10- to 40-fold with dbcAMP. Indomethacin treatment inhibited the stimulatory effect of dbcAMP; butyrate had no effect on PGF2α secretion. Treatment with LH had no effect on any of the PGs measured. In these experiments the secretion of progesterone appeared unrelated to any changes in the secretion of PGs. Thus it would appear that the production of progesterone by bovine luteal cells in culture is not related nor dependent upon the secretion of 6-keto-PGF1α, PGE2 or PGF2α, and that LH/cAMP does not regulate the secretion of PGs since LH had no effect on PG secretion and since the effects of dbcAMP appeared not to be through a cAMP-dependent pathway. J. Endocr. (1988) 118, 121–126