Thyrotropin Increases Prostaglandin Levels in Isolated Thyroid Cells

Open Access
Publisher Website
Google Scholar
Abstract
We have shown that two unrelated prostaglandin antagonists block both thyrotropin (TSH) and prostaglandins E (PGE1, PGE2) stimulation of thyroidal adenyl cyclase activation and cyclic 3′,5′-adenosine monophosphate (cAMP) formation, suggesting that prostaglandins play an important role in regulating thyroid function. To further explore this postulate, we measured prostaglandin content by radioimmunoassay in homogeneous bovine thyroid cell preparations in the presence and absence of TSH. Antibodies to albumin-conjugated PGE1 and PGF2α showed specificity for prostaglandins E and F, respectively, but reacted, albeit far less effectively, with heterologous prostaglandins. A double antibody system was used to separate free from antibody-bound PGE1-3H and PGF2α-3H. Thyroid cells were extracted with ethanol/ethyl acetate and the various prostaglandins separated on silicic acid columns. Recoveries of added PGE1-3H and PGF2α-3H through the extraction and separation procedures ranged from 50-80%. The sensitivity of the method was 10-50 pg. Basal thyroid cell content of PGE1 and PGF2α “equivalents” varied between cell preparations (range = 2-6 ng/0.2 ml cell suspension) but, in each instance, remained constant during 5-30-min incubations at 37°C. TSH, 10-100 mU/ml, increased the levels of cell PGE1 and PGF2α “equivalents” 30-80% above basal during 5-15-min incubations. The stimulatory effect was specific for TSH, no increase in PGE1 or PGF2α “equivalent” levels being seen with luteinizing hormone (LH), human growth hormone (HGH), adrenocorticotropic hormone (ACTH), or glucagon. These data support the thesis that prostaglandins may mediate TSH effects on thyroid.