Acceleration of oviductal transport of oocytes induced by estradiol in cycling rats is mediated by nongenomic stimulation of protein phosphorylation in the oviduct

Simple item page
dc.contributor.authorOrihuela, PA
dc.contributor.authorCroxatto, HB
dc.date.accessioned2025-01-21T01:30:42Z
dc.date.available2025-01-21T01:30:42Z
dc.date.issued2001
dc.description.abstractIn order to explore nongenomic actions of estradiol (E,) and progesterone (P-4) in the oviduct, we determined the effect of E-2 and P-4 on oviductal protein phosphorylation. Rats on Day 1 of the cycle (C1) or pregnancy (P1) were treated with E-2, P-4, or E-2 + P-4, and 0.5 h or 2.5 h later their oviducts were incubated in medium with P-32-orthophosphate for 2 h. Oviducts were homogenized and proteins were separated by SDS-PAGE. Following autoradiography, protein bands were quantitated by densitometry. The phosphorylation of some proteins was increased by hormonal treatments, exhibiting steroid specificity and different individual time courses. Possible mediation of the E-2 effect by mRNA synthesis or protein kinases A (PK-A) or C (PK-C) was then examined. Rats on C1 treated with E-2 also received an intrabursal (i.b.) injection of alpha -amanitin (Am), or the PK inhibitors H-89 or GF 109203X, and 0.5 h later their oviducts were incubated as above plus the corresponding inhibitors in the medium. increased incorporation of P-32 into total oviductal protein induced by E-2 was unchanged by Am, whereas it was completely suppressed by PK inhibitors. Local administration of H-89 was utilized to determine whether or not E-2-induced egg transport acceleration requires protein phosphorylation. Rats on C1 or P1 were treated with E-2 s.c. and H-89 Lb. The number and distribution of eggs in the genital tract assessed 24 h later showed that H-89 blocked the E-2-induced oviductal egg loss in cyclic rats and had no effect in mated rats. It is concluded that E-2 and P-4 change the pattern of oviductal protein phosphorylation. Estradiol increases oviductal protein phosphorylation in cyclic rats due to a nongenomic action mediated by PK-A and PK-C. In the abscence of mating, this action is essential for its oviductal transport accelerating effect. Mating changes the mechanism of action of E-2 in the oviduct by waiving this nongenomic action as a requirement for E-2-induced embryo transport acceleration.
dc.fuente.origenWOS
dc.identifier.issn0006-3363
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/96860
dc.identifier.wosidWOS:000171320400034
dc.issue.numero4
dc.language.isoen
dc.pagina.final1245
dc.pagina.inicio1238
dc.revistaBiology of reproduction
dc.rightsacceso restringido
dc.subjectestradiol
dc.subjectkinases
dc.subjectmechanisms of hormone action
dc.subjectoviduct
dc.subjectovum
dc.subjectprogesterone
dc.subjectsteroid hormones
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleAcceleration of oviductal transport of oocytes induced by estradiol in cycling rats is mediated by nongenomic stimulation of protein phosphorylation in the oviduct
dc.typeartículo
dc.volumen65
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
Files
Collections
Artículos de revistas