Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture.

Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture. Research Abstract Details 

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Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture. Abstract Text:

Maho Ishida,Tetsuo Mitsui,Koji Yamakawa,Nobuhiro Sugiyama,Wakaba Takahashi,Hiroki Shimura,Toyoshi Endo,Tetsurou Kobayashi,Jun Arita,Maho Ishida,Tetsuo Mitsui,Koji Yamakawa,Nobuhiro Sugiyama,Wakaba Takahashi,Hiroki Shimura,Toyoshi Endo,Tetsurou Kobayashi,Jun Arita,

Hypothalamic hormones, including dopamine, regulate critical functions of pituitary cells via the cAMP-protein kinase A (PKA) pathway. The PKA-downstream transcription factor cAMP response element (CRE)-binding protein (CREB) is an integrating molecule that is also activated by many other protein kinase pathways. We investigated the involvement of CREB in the regulation of cell proliferation and the PRL promoter of rat lactotrophs in primary cell culture. Recombinant adenoviruses were used for efficient gene delivery into pituitary cells. Bromocriptine, a dopaminergic agonist known to decrease intracellular cAMP concentrations, caused inhibition of PRL promoter activity and lactotroph proliferation, which was accompanied by decreases in CRE-mediated transcription and CREB phosphorylation in lactotrophs. Expression of a dominant-negative form of CREB (MCREB), which was effective in suppressing CRE-mediated transcription induced by the adenylate cyclase activator forskolin, inhibited basal and forskolin-induced PRL promoter activity and PRL mRNA expression. MCREB expression lowered basal proliferative levels and blocked forskolin-induced proliferation of lactotrophs. Insulin-like growth factor I (IGF-I), a potent mitogen in lactotrophs, did not affect intracellular cAMP concentrations but transiently increased lactotroph CREB phosphorylation. MCREB expression also inhibited IGF-I-induced lactotroph proliferation. These results suggest that CREB is involved in the regulation of cell proliferation and the PRL promoter in normal lactotrophs and that dopamine inhibition of these lactotroph functions is at least in part due to inhibition of the cAMP-PKA-CREB pathway.

Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture. Publishing Authors By Initials

M Ishida,T Mitsui,K Yamakawa,N Sugiyama,W Takahashi,H Shimura,T Endo,T Kobayashi,J Arita,M Ishida,T Mitsui,K Yamakawa,N Sugiyama,W Takahashi,H Shimura,T Endo,T Kobayashi,J Arita,

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Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: American journal of physiology. Endocrinology and

VOLUME: 293

Page Numbers: E1529-37

Journal Abbreviation: Am. J. Physiol. Endocrinol. Me

ISSN: 0193-1849

DAY: 9

MONTH: 10

YEAR: 2007

Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture. Information

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LANGUAGE: eng

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Grant and Affiliation Information for Involvement of cAMP response element-binding protein in the regulation of cell proliferation and the prolactin promoter of lactotrophs in primary culture.

AFFILIATION: Dept. of Physiology, Interdisciplinary Graduate School of Medicine and Engineering, Univ. of Yamanashi, 409-3898, Japan. jarita@yamanashi.ac.jp).

Country: United States

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MEDLINETA: Am J Physiol Endocrinol Metab

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