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Transforming growth factor-β stimulates vascular endothelial growth factor production by folliculostellate pituitary cells

MPG-Autoren

Renner,  U
Max Planck Institute of Psychiatry, Max Planck Society;

Lohrer,  P
Max Planck Institute of Psychiatry, Max Planck Society;

Schaaf,  L
Max Planck Institute of Psychiatry, Max Planck Society;

Feirer,  M
Max Planck Institute of Psychiatry, Max Planck Society;

Schmitt,  K
Max Planck Institute of Psychiatry, Max Planck Society;

Onofri,  C
Max Planck Institute of Psychiatry, Max Planck Society;

Arzt,  E
Max Planck Institute of Psychiatry, Max Planck Society;

Stalla,  GK
Max Planck Institute of Psychiatry, Max Planck Society;

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Zitation

Renner, U., Lohrer, P., Schaaf, L., Feirer, M., Schmitt, K., Onofri, C., et al. (2002). Transforming growth factor-β stimulates vascular endothelial growth factor production by folliculostellate pituitary cells. Endocrinology, 143(10), 3759-3765.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-A151-A
Zusammenfassung
TGF-beta isoforms are expressed in the anterior pituitary and modulate the growth and function of endocrine pituitary cells. Recently, TGF-beta has been shown to stimulate growth and basic fibroblast growth factor secretion in nonendocrine folliculostellate (FS) pituitary cells. We therefore studied whether the production of FS cell-derived vascular endothelial growth factor (VEGF), the most important regulator of vascular permeability and angiogenesis, is affected by TGF-beta. We observed by RT-PCR that TtT/GF cells, which are FS mouse pituitary tumor cells, synthesize TGF-beta1, -beta2, and - beta3. They also express TGF-beta receptors types 1 and 2, as well as Smad2, Smad3, and Smad4 proteins, which are essential for TGF-beta binding and signaling. Stimulation of TtT/GF cells with either TGF-beta1 or TGF-beta3, induced a rapid translocation of Smad2 into the cell nuclei. Both TGF-beta isoforms dose dependently stimulated VEGF production in TtT/GF cells, but not in lactosomatotroph GH3 cells. Time-course studies and suppression of TGF-beta-induced VEGF production by cycloheximide suggest that TGF-beta induces de novo synthesis of VEGF in folliculostellate cells, which is completely blocked by dexamethasone. In primary rat pituitary cell cultures, TGF- beta1 and -beta3 stimulated VEGF production. TGF-beta stimulation of VEGF production by folliculostellate cells could modulate intrapituitary vascular permeability and integrity as well as angiogenesis in an auto-/paracrine manne