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This version published online on September 1, 2005
Molecular Endocrinology, doi:10.1210/me.2005-0195
Molecular Endocrinology Vol. 0, No. 2005 200501951-
doi:10.1210/me.2005-0195
Copyright © 2005 by the Endocrine Society.
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Submitted on May 17, 2005
Accepted on August 23, 2005

Hypothalamic CREB loss causes anterior pituitary hypoplasia and dwarfism in mice

Theo Mantamadiotis*, Oliver Kretz, Stephanie Ridder, Susanne C. Bleckmann, Dagmar Bock, Hermann-Josef Gröne, Jordane Malaterre, Sebastian Dworkin, Robert G. Ramsay, and Günther Schütz

Molecular Biology of the Cell I (T.M., S.R., O.K., S.C.B., D.C., G.S.), Department of Cellular and Molecular Pathology (H.J.G), Deutsches Krebsforschungszentrum, 69120 Heidelberg, Institute of Anatomy and Cell Biology, University of Freiburg (O.K.), Germany, Peter MacCallum Cancer Centre (T.M., J.M., S.D., R.G.R), East Melbourne, 3002, Australia

* To whom correspondence should be addressed. E-mail: theo.mantamadiotis{at}petermac.org.

The principal regulation of body growth is via a cascade of hormone signals emanating from the hypothalamus, by release of GH releasing hormone (GHRH), which then directs the somatotroph cells of the pituitary to release GH (GH) into the blood stream. This in turn leads to activation of Stat5- dependent expression of genes such as IGF-I in hepatocytes, acid labile substance and serine protease inhibitor 2.1, resulting in body growth. Here, using conditional cAMP response element binding (CREB) protein mutant mice, we show that loss of the CREB transcription factor in the brain but not the pituitary, results in reduced postnatal growth consistent with dwarfism caused by GH deficiency. We demonstrate that although there appears to be no significant impact upon the expression of GHRH mRNA in CREB mutant mice, the amount of GHRH peptide is reduced. These findings show that CREB is required for the efficient production of GHRH in hypothalamus, in addition to its previously reported role in pituitary GH production and somatotroph expansion.
Key words: CREB • growth • transcription • transgenic • GHRH • hypothalamic




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