Estrogen receptor, cyclic adenosine monophosphate, and protein kinase A are involved in the nongenomic pathway by which estradiol accelerates oviductal oocyte transport in cyclic rats

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dc.contributor.authorOrihuela, PA
dc.contributor.authorParada-Bustamante, A
dc.contributor.authorCortés, PP
dc.contributor.authorGatica, C
dc.contributor.authorCroxatto, HB
dc.date.accessioned2025-01-21T01:09:33Z
dc.date.available2025-01-21T01:09:33Z
dc.date.issued2003
dc.description.abstractThis investigation examined the role of estrogen receptor (ER) on the stimulatory effect of estradiol (E) on protein phosphorylation in the oviduct as well as on E-2-induced acceleration of oviductal oocyte transport in cyclic rats. Estrous rats were injected with E-2 s.c. and with the ER antagonist 10 182 780 intrabursally (i.b.), and 6 h later, oviducts were excised and protein phosphorylation was determined by Western blot analysis. ICI 182780 inhibited the E-2-induced phosphorylation of some oviductal proteins. Other estrous rats were treated with E-2 s.c. and ICI 182 780 i.b. The number of eggs in the oviduct, assessed 24 h later, showed that ICI 182 780 blocked the E-2-induced egg transport acceleration. The possible involvement of adenylyl cyclase, protein kinase A (PK-A), protein kinase C (PK-C), or tyrosine kinases on egg transport acceleration induced by E-2 was then examined. Selective inhibitors of adenylyl cyclase or PK-A inhibited the E-2-induced egg transport acceleration, whereas PK-C or tyrosine kinase inhibitors had no effect. Furthermore, forskolin, an adenylyl cyclase activator, mimicked the effect of E-2 on ovum transport and E, increased the level of cAMP in the oviduct of cycling rats. Finally, we measured PK-A activity in vitro in the presence of E-2 or E-2-ER complex. Activity of PK-A in the presence of E-2 or E-2-ER was similar to PK-A alone, showing that E-2 or E-2-ER did not directly activate PK-A. We conclude that the nongenomic pathway by which E-2 accelerates oviductal egg transport in the rat requires absolute participation of ER and cAMP and partial participation of PK-A signaling pathways in the oviduct.
dc.fuente.origenWOS
dc.identifier.doi10.1095/biolreprod.102.011395
dc.identifier.issn0006-3363
dc.identifier.urihttps://doi.org/10.1095/biolreprod.102.011395
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/96596
dc.identifier.wosidWOS:000181844400019
dc.issue.numero4
dc.language.isoen
dc.pagina.final1231
dc.pagina.inicio1225
dc.revistaBiology of reproduction
dc.rightsacceso restringido
dc.subjectcyclic adenosine monophosphate
dc.subjectestradiol
dc.subjectestradiol receptor
dc.subjectoviduct
dc.subjectovum pick-up/transport
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleEstrogen receptor, cyclic adenosine monophosphate, and protein kinase A are involved in the nongenomic pathway by which estradiol accelerates oviductal oocyte transport in cyclic rats
dc.typeartículo
dc.volumen68
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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