HEREÑÚ CLAUDIA BEATRIZ
Congresos y reuniones científicas
Título:
Construction of an adenoviral vector expressing TGFbeta3 and its use for the study of the genesis of prolactinomas
Autor/es:
HEREÑÚ C.B #*.;; CUI PING CHEN #;; OMAR RIMOLDI*;; RODOLFO GOYA*;; DIPAK SARKAR #.
Lugar:
Iguazú, Argentina
Reunión:
Congreso; Congress Pituitary Today: Molecular, Physiological and Clinical aspects( 2005); 2005
Resumen:

Abstract: In order to study the in vivo effects of TGFb3 overexpression in the rat pituitary under different experimental conditions, we undertook to construct an adenoviral vector expressing the cDNA encoding rat TGFb3. Under basal conditions, PRL cells are under a tonic inhibitory autofeedback of TGFb1 acting on the TGFb II and I receptors.When estrogen appears in high levels, it stimulates PRL cells to release high levels of TGFb3 wich then acts on TGF receptors II on Folliculo-Stellate cells inducing the production and release of basic Fibroblast Growth Factor . This factor in turn acts on PRL cells to stimulate both cell proliferation and PRL secretion. With the purpose to verify if the vector worked OK, we incubated FS cell cultures with our vector and measured the release of TGFb3 in the supernatants. We could see that the vector worked OK and was able to induce high levels of expression and release of transgenic TGFb3. We moved then to the in vivo scenario in order to induce TGFb3 over expression in estrogen-induced pituitary prolactinomas. To inject our vectors into the pituitary we performed bilateral stereotaxic injections, delivering 1 ul of vector suspension at the appropriate coordinates. From the results of this work we conclude :1- TGFb3 adenoviral vector is an effective tool for TGFb3 gene.transfer in pituitary cells both in vitro and in vivo. 2 - The inhibitory effect of transgenic TGFb3 on serum PRL levels and pituitary weight in OVX rats suggests that in the absence of E2, the TbRI/ TbRII system is functional and thereforeTGFb3 stimulates the TGFb1 tonic inhibitory autofeedback mechanism. 3-  On the contrary, the stimulatory effect of transgenic TGFb3 on PRL levels and pituitary weight in E2 treated rats suggests that in the presence of high E2 levels, TbRI/ TbRII system is not functional and therefore TGFb3 acts on FS cells to induce bFGF release and subsequent PRL cell stimulation .4- These results are consistent with the proposed TGFb3 role in the mechanism for the genesis of E2-induced prolactinomas.