Rodgers R J, O'Shea J D, Findlay J K
J Reprod Fertil. 1985 Sep;75(1):85-94. doi: 10.1530/jrf.0.0750085.
Corpora lutea from cyclic ewes were dissociated by collagenase and trypsin/EGTA treatments, and enriched fractions of small and large luteal cells were prepared on gradients of Ficoll. These fractions were incubated separately or remixed before incubation. Colchicine, cytochalasin B and the calcium channel-blocker verapamil significantly reduced progesterone production by both small and large luteal cell fractions, while isoprenaline stimulated an increase in progesterone production by large luteal cell fractions only. When fractions of small and large luteal cells were remixed, no more and no less progesterone was produced than would have been predicted from equivalent fractions incubated separately. There was therefore no evidence of synergism between small and large luteal cells in the production of progesterone. Prostaglandin F-2 alpha, which can inhibit LH-stimulated progesterone production by ovine luteal tissue in vitro, had no effect on LH-stimulated progesterone production by small luteal cell fractions, but significantly inhibited that by enriched fractions of large luteal cells. Since large luteal cell fractions were contaminated with small luteal cells, which are probably responsible for the progesterone-secretory response of these fractions to LH, it was concluded that the inhibition of LH-stimulated progesterone production by small luteal cells is dependent on the presence of large luteal cells. Oxytocin added to large and small luteal cell fractions did not affect progesterone production by either fraction. It was therefore concluded that the inhibitory action of PGF-2 alpha on LH-stimulated progesterone production may require the interaction of large and small luteal cells, but that oxytocin is not likely to be an intermediary in this interaction.
通过胶原酶以及胰蛋白酶/乙二醇双四乙酸处理，使处于发情周期的母羊的黄体解离，并在菲可梯度上制备大小黄体细胞的富集组分。这些组分单独孵育或在孵育前重新混合。秋水仙碱、细胞松弛素B以及钙通道阻滞剂维拉帕米显著降低了大小黄体细胞组分的孕酮生成，而异丙肾上腺素仅刺激大黄体细胞组分的孕酮生成增加。当大小黄体细胞组分重新混合时，产生的孕酮量并不比单独孵育同等组分时预测的量多或少。因此，在孕酮生成方面，大小黄体细胞之间没有协同作用的证据。前列腺素F-2α在体外可抑制绵羊黄体组织中促黄体生成素（LH）刺激的孕酮生成，但对小黄体细胞组分中LH刺激的孕酮生成没有影响，却显著抑制了大黄体细胞富集组分的这种生成。由于大黄体细胞组分被小黄体细胞污染，而小黄体细胞可能是这些组分对LH分泌孕酮反应的原因，因此得出结论，小黄体细胞对LH刺激的孕酮生成的抑制依赖于大黄体细胞的存在。向大小黄体细胞组分中添加催产素对任何一组的孕酮生成均无影响。因此得出结论，PGF-2α对LH刺激的孕酮生成的抑制作用可能需要大小黄体细胞的相互作用，但催产素不太可能是这种相互作用的中介物。
