SciELO - Scientific Electronic Library Online

 
vol.141 issue4Flouroquinolone activity in clinical isolates of Streptococcus pneumoniae with different susceptibility to penicilline: An epidemiological study in five cities of MexicoTreatment of hyaline membrane disease in the preterm newborn with exogenous lung surfanctant. A controlled study author indexsubject indexsearch form
Home Pagealphabetic serial listing  

Services on Demand

Journal

Article

Indicators

Related links

  • Have no similar articlesSimilars in SciELO

Share


Gaceta médica de México

On-line version ISSN 2696-1288Print version ISSN 0016-3813

Abstract

LARREA, Fernando; SANCHEZ-GONZALEZ, Sergio; GARCIA-BECERRA, Rocío  and  MENDEZ, Isabel. Sites of prolactin inhibition on gonadotropin-induced estrogen production in cultured rat granulosa cells. Gac. Méd. Méx [online]. 2005, vol.141, n.4, pp.259-266. ISSN 2696-1288.

We studied the sites of prolactin inhibition upon FSH induced ovarian steroidogenesis and the ability of prolactin (Prl) to inhibit the synthesis of estradiol and cAMP accumulation under the stimulation of FSH or cAMP dependent activators. The participation of other signal pathways such as PKC and Gi proteins on the inhibitory actions of Prl was also investigated using calfostine C andpertusis toxin as inhibitors. Results showed a dose dependent prolactin decrease in FSH-induced estradiol and cAMP production prior and after the generation of the cyclic nucleotide by a mechanism involving the catalytic subunit of adenyl cyclase and/or through activation of PKC or by the interaction with pertusin toxin sensitive G proteins. Our results suggest a mechanism by which G protein coupled receptors are linked with those coupled with tyrosine kinase through the involvement of a Gi protein mediated mechanism.

Keywords : Prolactin; FSH; mechanisms of action; G proteins; granulosa cells; receptors.

        · abstract in Spanish     · text in Spanish

 

Creative Commons License All the contents of this journal, except where otherwise noted, is licensed under a Creative Commons Attribution License