Effect of hyperthyroidism (HT) on luteal expression of PRL signaling molecules on late pregnant rats.

NAVAS PB; PENNACCHIO GE; HAPON MB; VALDEZ SR; JAHN GA

Mendoza - Argentina

Congreso; XXVIII Reunión Científica de la Sociedad de Biología de Cuyo,; 2010

Sociedad de Biología de Cuyo

Thyroid disorders cause pregnancy disorders and lactation failure. In pregnant rats HT advances luteolysis, which causes premature delivery and increases serum PRL. The advanced luteolysis is caused by increased luteal and serum prostaglandin F2α, a luteolytic factor, but intraluteal mechanisms, such as alterations in PRL (a luteotrophic factor) signaling may be involved. We explored, by real time PCR, luteal mRNA expression of PRL receptor (PRLR), STAT5b (mediator of PRL signaling), SOCS-1, SOCS-3 and CIS (suppressors of PRL signaling induced by PRL) on rats on days 19 (G19), 20 (G20) and 21 (G21) of pregnancy treated with vehicle (Co) or T4 (HT, 250 µg/kg/day). In Co rats expression of PRLR, STAT5b, SOCS1 and CIS fell significantly on G21 compared with G19, while in HT rats there was a significant increase in their expression in G21 compared with Co rats, except SOCS3, that did not change, and PRLR that fell in both groups on G20 and G21. These results suggest that HT tends to maintain elevated expression of suppressors of PRL signaling on G20 and G21, facilitating luteolysis. On the other hand, the increased circulating PRL of HT rats on G21 may be the cause of the increased expression of STAT5b on G21 that in turn may contribute to maintain high SOCS and CIS expression in the presence of very low PRLR expression.