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  Involvement of bone morphogenetic protein 4 (BMP-4) in pituitary prolactinoma pathogenesis through a Smad/estrogen receptor crosstalk

Paez-Pereda, M., Giacomini, D., Refojo, D., Nagashima, A., Hopfner, U., Grübler, Y., et al. (2003). Involvement of bone morphogenetic protein 4 (BMP-4) in pituitary prolactinoma pathogenesis through a Smad/estrogen receptor crosstalk. Proceedings of the National Academy of Sciences of the United States of America, 100(3), 1034-1039.

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Datensatz-Permalink: https://hdl.handle.net/11858/00-001M-0000-000E-9F39-F Versions-Permalink: https://hdl.handle.net/11858/00-001M-0000-000E-9F3A-D
Genre: Zeitschriftenartikel
Alternativer Titel : Proc. Natl. Acad. Sci. U. S. A.

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 Urheber:
Paez-Pereda, M, Autor
Giacomini, D, Autor
Refojo, D, Autor
Nagashima, AC, Autor
Hopfner, U, Autor
Grübler, Y, Autor
Chervin, A, Autor
Goldberg, V, Autor
Goya, R, Autor
Hentges, ST, Autor
Low, MJ, Autor
Holsboer, F1, Autor
Stalla, GK, Autor
Arzt, E, Autor
Affiliations:
1Max Planck Institute of Psychiatry, Max Planck Society, ou_1607137              

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Schlagwörter: signal transduction; pituitary neoplasms
 Zusammenfassung: Pituitary tumor development involves clonal expansion stimulated by hormones and growth factors/cytokines. Using mRNA differential display, we found that the bone morphogenetic protein (BMP) inhibitor noggin is down-regulated in prolactinomas from dopamine D2-receptor-deficient mice. BMP-4 is overexpressed in prolactinomas taken from dopamine D2- receptor-deficient female mice, but expression of the highly homologous BMP-2 does not differ in normal pituitary tissue and prolactinomas. BMP-4 is overexpressed in other prolactinoma models, including estradiol-induced rat prolactinomas and human prolactinomas, compared with normal tissue and other pituitary adenoma types (Western blot analysis of 48 tumors). BMP-4 stimulates, and noggin blocks, cell proliferation and the expression of c-Myc in human prolactinomas, whereas BMP-4 has no action in other human pituitary tumors. GH3 cells stably transfected with a dominant negative of Smad4 (Smad4dn; a BMP signal cotransducer) or noggin have reduced tumorigenicity in nude mice. Tumor growth recovered in vivo when the Smad4dn expression was lost, proving that BMP-4/Smad4 are involved in tumor development in vivo. BMP-4 and estrogens act through overlapping intracellular signaling mechanisms on GH3 cell proliferation and c-myc expression: they had additive effects at low concentrations but not at saturating doses, and their action was inhibited by blocking either pathway with the reciprocal antagonist (i.e., BMP-4 with ICI 182780 or 17beta- estradiol with Smad4dn). Furthermore, coimmunoprecipitation studies demonstrate that under BMP-4 stimulation Smad4 and Smad1 physically interact with the estrogen receptor. This previously undescribed prolactinoma pathogenesis mechanism may participate in tumorigenicity in other cells where estrogens and the type beta transforming growth factor family have important roles

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Sprache(n): eng - English
 Datum: 2003-02-01
 Publikationsstatus: Erschienen
 Seiten: -
 Ort, Verlag, Ausgabe: -
 Inhaltsverzeichnis: -
 Art der Begutachtung: Expertenbegutachtung
 Identifikatoren: eDoc: 3994
ISI: 000180838100049
 Art des Abschluß: -

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Titel: Proceedings of the National Academy of Sciences of the United States of America
  Alternativer Titel : Proc. Natl. Acad. Sci. U. S. A.
Genre der Quelle: Zeitschrift
 Urheber:
Affiliations:
Ort, Verlag, Ausgabe: -
Seiten: - Band / Heft: 100 (3) Artikelnummer: - Start- / Endseite: 1034 - 1039 Identifikator: ISSN: 0027-8424