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Am J Physiol Endocrinol Metab 281: E1316-E1325, 2001;
0193-1849/01 $5.00
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Vol. 281, Issue 6, E1316-E1325, December 2001

Molecular mechanisms involved in gastrin-mediated regulation of cAMP-responsive promoter elements

Liv Thommesen1, Eva Hofsli1, Ruth H. Paulssen3, Marit W. Anthonsen2, and Astrid Lægreid1

1 Department of Physiology and Biomedical Engineering, 2 Faculty of Chemistry and Biology, Norwegian University of Science and Technology, N-7489 Trondheim; and 3 Department of Clinical Medicine, Tromsø University, N-9037 Tromsø, Norway

In the present study, we explore the role of cAMP-responsive (CRE) promoter elements in gastrin-mediated gene activation. By using the minimal CRE promoter reporter plasmid, pCRELuc, we show that gastrin can activate CRE. This activation is blocked by H-89 and GF 109203x, which inhibit protein kinases A and C, respectively. Moreover, Ca2+-activated pathways seem to be involved, because the calmodulin inhibitor W-7 reduced gastrin-mediated activation of pCRELuc. Deletion of CRE from the c-fos promoter rendered this promoter completely unresponsive to gastrin, indicating that CRE plays a central role in c-fos transactivation. Interestingly, gastrin-induced expression of the inducible cAMP early repressor (ICER), a gene that is known to be regulated by CRE promoter elements, was not reduced by H-89, W-7, or GF 109203x. Furthermore, bandshift analyses indicated that the region of the ICER promoter containing the CRE-like elements CARE 3-4 binds transcription factors that are not members of the CRE-binding protein-CRE modulator protein-activating transcription factor, or CREB/CREM/ATF-1, family. Our results underline the significance of the CRE promoter element in gastrin-mediated gene regulation and indicate that a variety of signaling mechanisms are involved, depending on the CRE promoter context.

3',5'-cyclic adenosine monophosphate; inducible cyclic adenosine monophosphate early repressor; signal transduction; gastrin;


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