CROSSTALK BETWEEN PROLACTIN AND THYROID HORMONES SIGNALING IN CORPUS LUTEUM AT THE END OF PREGNANCY IN THE RAT

NASIF DL; CAMPO VERDE ARBOCCO F; GAMARRA-LUQUES CD; JAHN GA; HAPON MB

Estancia Grande

Congreso; XXXII REUNIÓN CIENTÍFICA ANUAL DE LA SOCIEDAD DE BIOLOGÍA DE CUYO; 2014

SOCIEDAD DE BIOLOGÍA DE CUYO

The corpus luteum (CL) is an ephemeral endocrine gland that secretes progesterone (P4) throughout the entire length of gestation in the rat and plays a central role in the maintenance of pregnancy. P4 secretion is supported by prolactin (PRL) and placental lactogens (PL) via PRL receptor (PRLR) and JAK2/STAT pathway. On the other hand, PRL signaling suppresses 20 hydroxysteroid dehydrogenase (20HSD) which metabolizes P4 to inactive 20 -hydroxyprogesterone. At the end of pregnancy, the surge of uterine prostaglandin F2 (PGF2) induces expression of members of the suppressors of cytokine signaling (SOCS), that in turn inhibit PRLR signal transduction in the CL triggering luteolysis and the inactivation of P4. Our previous results demonstrated that hypothyroidism (hypoT) impairs CL function at the end of gestation delaying the surge of PGF2 and 20HSD expression, thus postponing the onset of parturition in the rat. The aim of this study was to evaluate the effect of hypoT on the expression of the components of PRLR pathway in the CL at the end ofpregnancy in the rat. Experimental hypoT was induced in Wistar rats by the chronic administration of the antithyroid drug propylthiouracil. The RNAm expression of SOCS1 and 3, CIS, PRLR, STAT5B and 20HSD was determined by RTqPCR and SOCS3, STAT5B, pSTAT5B and CIS protein expression by Western blot in the CL at the end of pregnancy. Our results demonstrated that hypoT diminished protein expression of SOCS3 and increased the ratio of pSTAT5B/STAT5B level at p