Effect of hyperthyroidism (HT) on PRL signaling molecules on late pregnancy

PAOLA B. NAVAS; PENNACCHIO GE; HAPON MB; VALDEZ SR; JAHN GA

Mendoza Argentina

Congreso; Sociedad de Biologia de Cuyo; 2010

Sociedad Biologia de Cuyo

Thyroid disorders compromise fertility in women in reproductive age and cause pregnancy disorders and lactation failure. In pregnant rats HT advances luteolysis, which causes premature delivery and increase in 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 the changes in luteal mRNA expression of PRL receptor (PRLR), STAT5b (mediator of PRL signaling), SOCS-1, SOCS-3 and CIS (suppressors of PRL signaling and 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 STAT5b, SOCS1, SOCS3 and CIS fell significantly on G21 compared with G19, while in HT rats there was a tendency to decrease on G19 in all these factors and a significant increase in their expression in G21 compared with Co rats, except SOCS1 in which the increase did not reach significance. These results suggest that HT tends to advance the decrease in the expression of luteal factors mediating PRL signaling observed at the end of pregnancy, that are involved in the luteolytic process, but that this effect is very modest. On the other hand, the increased circulating PRL of HT rats on G21 may be the cause of the increased expression of these factors observed on G21.