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Updated: Aug 19, 2026

Screening for Phytoestrogens using a Cell-based Estrogen Receptor β Reporter Assay
Published on: June 7, 2020
Is thyroid hormone a modulator of estrogen receptor in porcine follicular cells?
1Laboratory of Reproductive Physiology and Toxicology, Department of Physiology, Institute of Zoology, Jagiellonian University, Kraków, Poland. greg@zuk.iz.uj.udu.pl
Objective:
To examine whether the action of triiodothyronine on aromatase activity in porcine follicular cells is related to the modulation of estradiol receptor.
Methods:
Medium and large preovulatory follicles were incubated in Parker medium (M199) supplemented with 5 % of calf serum as a control medium or with addition of triiodothyronine (T3; 10 -9 M), tamoxifen (TMX; 0.1 mM ) or T3+TMX. The media were collected after 48 h, and assayed for progesterone (P4) and estradiol (E2) secretion by RIA.
Results:
T3 added to the medium decreased E2 secretion by both medium and large preovulatory follicles (119.7 % and 123.8 %, respectively; P<0.05). In contrast, T3 increased the secretion of P4 by medium (136 %; P<0. 05), while decreased the P4 secretion by large preovulatory follicles (123 %; P<0.05). The effect of TMX added alone was also dependent on follicular development. Estradiol secretion by medium follicles was 2.5 fold higher (p<0.01) than in control and 2.9 fold higher (P<0.01) than in T3 treated cells. In preovulatory follicles basal E2 secretion was not affected by TMX, while 1.2 fold higher (P<0.05) secretion compared to T3 treated cells was noted. On the other hand, TMX suppressed basal P4 secretion in medium and preovulatory follicles 1.5 fold (P<0.01) and 1.3 fold (P<0.05), respectively. The same phenomenon was observed in T3 treated cells. TMX added to the culture media decreased P4 secretion by medium follicles 1.8 fold (P<0.01) and that by preovulatory follicles 1.3 fold (P<0.05).
Conclusions:
The reversed T3 action on estradiol secretion by both medium (P<0.05) and large preovulatory (P<0.01) follicles in TMX treated follicles suggests the up-regulation of ER by triidothyronine.
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