QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: mol.106.025064v1 70/1/154    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by González-Arenas, A. Articles by García-Sáinz, J. A. Search for Related Content PubMed PubMed Citation Articles by González-Arenas, A. Articles by García-Sáinz, J. A.

Estrogens Cross-Talk to _1b-Adrenergic Receptors

Instituto de Fisiología Celular, Universidad Nacional Autónoma de México, Ciudad de México, México

-Estradiol induced _1b-adrenergic receptor desensitization in U373 MG cells stably expressing _1b-adrenoceptors, as evidenced by a reduction in the adrenergic-mediated Ca²⁺ mobilization; desensitization was associated with receptor phosphorylation and internalization. These effects of -estradiol were rapid (taking place during 15 min) and were blocked by the estrogen receptor antagonist ICI 182,780 (faslodex). Likewise, inhibitors of phosphoinositide 3-kinase [wortmannin and 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002)] and of protein kinase C [staurosporine, 3-[1-[3-(amidinothio)propyl-1H-indol-3-yl]-3-(1-methyl-1H-indol-3-yl) maleimide (Ro31-8220), and rottlerin] blocked the desensitization and phosphorylation of _1b-adrenoceptors induced by estradiol. The formation of a complex was suggested by coimmunoprecipitation assays. The regulatory and catalytic subunits of phosphoinositide 3-kinase (p85 and p110) and protein kinase C were associated with _1b-adrenoceptors in the absence of stimulus, and such association further increased in a dynamic fashion in response to -estradiol. In cells cotransfected with the estrogen receptor and _1b-adrenoceptors, -estradiol induced phosphorylation, desensitization and internalization of the adrenergic receptors; pretreatment with ICI 182,780 inhibited these effects. Our data support the idea that estrogens modulate _1b-adrenergic action through estrogen receptor .

Address correspondence to: J. Adolfo García-Sáinz, Instituto de Fisiología Celular, UNAM, Ap. postal 70–248, México D. F. 04510. E-mail: agarcia{at}ifc.unam.mx