Differential Action of Sulfated Glycosaminoglycans on Follicle-Stimulating Hormone-Induced Functions of Cumuli Oophori Isolated from Mice

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Abstract
It was shown previously that FSH-induced cumulus expansion was suppressed by sulfated glycosaminoglycans (GAG), and it was suggested that the action of the GAG was distal to FSH-stimulated elevation of intracellular cAMP. To test this hypothesis for the site of action, the effects of sulfated GAG on FSH-stimulated intracellular cAMP levels were measured by radioimmunoassay. The sulfated GAG, heparin and chondroitin sulfate B, used at concentrations that completely inhibit cumulus expansion (100 .mu.g/ml and 5 mg/ml, respectively), did not inhibit FSH-stimulated elevation of intracellular cAMP. The effects of sulfated GAG on FSH-stimulated incorporation of 3H-choline into cumulus cell-oocyte complexes were determined to further assess the actions of these GAG on cumulus cell functions. Highly purified FSH, but not highly purified luteinizing hormone (LH) or human chorionic gonadotropin (hCG), stimulated the incorporation of 3H-choline into isolated cumulus cell-oocyte complexes. The incorporation of 3H-choline into the complexes was almost entirely the result of cumulus cell, rather than oocyte, function. About 25-30% of the radiolabel was transformed from the cumulus cells to the oocytes. FSH-stimulated 3H-choline incorporation appeared to be mediated by cAMP since incorporation was also stimulated by dibutyryl cAMP (dbcAMP), cholera toxin and 3-isobutyl-l-methyl-xanthine. However, unlike the inhibitory effect of sulfated GAG on FSH-stimulated cumulus expansion, neither heparin (100 .mu.g/ml) nor chondroitin sulfate B (5 mg/ml) inhibited 3H-choline incorporation into cumulus cell-oocyte complexes. In addition, heparin did not inhibit FSH-stimulated anabolism of the 3H-choline into phosphatidylcholine. The action of sulfated GAG on FSH-stimulated functions of cumulus cells is differential and its inhibitory action on cumulus expansion is exerted distally to FSH-stimulated elevation of intracellular cAMP.