INVESTIGADORES
JAHN Graciela Alma
artículos
Título:
Hypothyroidism prolongs corpus luteum function in the pregnant rat through modulation of luteotrophic and luteolytic signals.
Autor/es:
HAPON, M.B.; BONAFEDE, M.; EZQUER, M.; MOTTA, A.B.; JAHN, G.A.
Revista:
REPRODUCTION
Editorial:
BioScientifica
Referencias:
Lugar: Bristol; Año: 2007 vol. 133 p. 197 - 205
ISSN:
1470-1626
Resumen:
It has been shown that hypothyroidism in the rat produces a prolongation of pregnancy associated with a delay in the fall of circulating progesterone (P4) at term. The aim of the present work is to determine whether the delayed P4 decline in hypothyroid mother rats is due to a retarded induction of P4 degradation to 20aOH P4 or to a stimulation of its synthesis, and to investigate the possible mechanisms that may underlie the altered luteal function. We determined by RIA the circulating profile of the hormones (TSH, PRL, LH, P4, PGF2a and PGE2) involved in luteal regulation at the end of pregnancy and, by semiquantitative RT-PCR, the expression of factors involved in P4 synthesis (CytP450scc, StAR, 3bHSD, PRLR) and metabolism (20aHSD, PGF2a, PGF2aR, iNOS and COX2). Our results show that the delay in P4 decline and parturition is the resultant of retarded luteal regression, caused by a combination of decreases in luteolytic factors, mainly luteal PGF2a, iNOS mRNA expression and also circulating LH, and increased synthesis or action of luteotrophic factors, such as luteal and circulating PGE2 and circulating PRL. All these changes may be direct causes of the decreased 20aHSD mRNA and protein (measured by western blot analysis) expression, which, in the presence of unchanged expression of the factors involved in P4 synthesis results in elevated luteal and circulating P4 that prolonged pregnancy and also may favour longer survival of the corpus luteum.