Abstract:
:In previous studies we demonstrated that IGF-I induces proliferation of pituitary lactotrophs. In addition to its mitotrophic actions, IGF-I is known to prevent apoptosis induced by diverse stimuli in several cell types. In this study, we investigated the action of IGF-I on pituitary cell survival and the intracellular signaling transduction pathway implicated in this effect. Treatment of cultured male rat pituitary cells with IGF-I (10(-7) M) for 24 h prevented pituitary cell death induced by serum deprivation. The protective effect of IGF-I was blocked by phosphoinositide 3-kinase (PI3-kinase) inhibitor, LY294002, but was unaffected by PD98059, which inhibits MAP/ERK kinase (MEK1). IGF-I activation of PI3-kinase induced the phosphorylation and activation of the serine/threonine kinase Akt. Moreover, IGF-I increased the phosphorylation of the pro-apoptotic factor Bad and the levels of the anti-apoptotic protein Bcl-2 through the PI3-kinase pathway in primary pituitary cells.
journal_name
J Mol Endocrinoljournal_title
Journal of molecular endocrinologyauthors
Fernández M,Sánchez-Franco F,Palacios N,Sánchez I,Fernández C,Cacicedo Ldoi
10.1677/jme.0.0330155subject
Has Abstractpub_date
2004-08-01 00:00:00pages
155-63issue
1eissn
0952-5041issn
1479-6813journal_volume
33pub_type
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