Expression of members of the prolactin signaling pathway in rat hypothalamus and regulation by thyroid hormones on late pregnancy

PENNACCHIO GISELA E; NAVAS PAOLA B; SOAJE MARTA; JAHN GRACIELA A; VALDEZ SUSANA R

Mendoza

Congreso; Sociedad de Biología de Cuyo; 2010

Sociedad de Biología de Cuyo y Secretaría de Ciencia, Técnica y Posgrado de UNCuyo.

@font-face { font-family: "Cambria"; }p.MsoNormal, li.MsoNormal, div.MsoNormal { margin: 0cm 0cm 0.0001pt; font-size: 12pt; font-family: "Times New Roman"; }div.Section1 { page: Section1; } Thyroid disorders compromise fertility in women in reproductive age and cause pregnancy disorders and lactation failure. Hyperthyroidism alters prolactin (PRL) secretion at the end of pregnancy, advances delivery and impairs lactation in rats. Using real time quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) we explored the changes in mRNA expression of long PRL receptor (PRLR), STAT5b (required for the negative-feedback action of PRL on hypothalamic dopaminergic neurons), SOCS-1, SOCS-3, CIS (proteins that disrupt downstream STAT translocation to the nucleus to suppress prolactin signaling) in medial basal hypothalamus (MBH) during late pregnancy in hyperthyroid and normal rats. Thyroxin-treated (HT, 250 µg/kg/day) or vehicle-treated (Co) rats were mated 8 days after the start of treatment and killed at days 20 (G20) and 21 (G21) of pregnancy. Serum concentrations of thyroid hormones increased in HT rats. HT increased MBH PRLR on G21 (1.01±0.12 vs Co 0.62±0.12, p<0.05). STAT5b mRNA increased in HT rats on G20 and G21 (G20 Co: 1.00± 0.15, HT: 2.2 ± 0.17; G21Co: 0.6± 0.19, HT: 1.6± 0.27, p<0.05). CIS and SOCS-1 expression did not change but SOCS-3 mRNA increased in HT at G20 (G20 HT 2.75 ±0.20 vs G20 Co 0.92±0.19, p< 0.05) and fell on G21 to values similar to Co rats (G21 Co 0.45±0.09 vs G21 HT 0.59±0.09 ns). These results indicate that PRL-R, STAT5b and SOCS-3 expression are differentially regulated in HMB by thyroid hormones.