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Submitted on September 23, 2005
Accepted on March 8, 2006
Department of Endocrinology (M.Y.), Toyota Memorial Hospital, Toyota 471-8513; Department of Endocrinology, Metabolism, and Nephrology (Y.I., K.H.), Kochi Medical School, Kochi University, Kohasu, Oko-cho, Nankoku 783-8505; Department of Endocrinology and Diabetes (M.Y., M.A., Y.O.), Departmernt of Clinical Pathophysiology (S.T.), Nagoya University Graduate School of Medicine, Nagoya 466-8550; Laboratory of Information Biology (K.I.), Graduate School of Information Science, Tohoku University, Sendai 980-8579; Japan
* To whom correspondence should be addressed. E-mail: masanori_yoshida{at}mail.toyota.co.jp.
Arginine vasopressin (AVP) is expressed in paraventricular, supraoptic, and suprachiasmatic neuclei of the hypothalamus, where the transcription of AVP gene is activated by various forms of stress, such as hyperosmolality, inflammation, and photic stimulation. In vasopressinergic neurons, the expression of the Fos/Jun family proteins are known to be rapidly induced after these stimuli as well. However, it is still unknown whether these proteins actually mediate AVP gene expression. In this study, we examined in vitro the role of Fos/Jun protein in the transcriptional regulation of AVP gene using the BE (2)M17 neuroblastoma cell line. We found that 5'-promoter activity of the rat AVP gene (-803/+26) markedly increased when all the combinations of the Fos/Jun family proteins are overexpressed. Co-expression of the CREB-binding protein (CBP) and steroid receptor coactivator-1a (SRC-1a) further enhanced the Fos/Jun-mediated transcription. Using site-directed mutagenesis and electromobility shift assay techniques, we identified AP1-like element (-134/-128, TGAATCA) in the AVP gene 5'-promoter region, which is the sole responsible site for the Fos/Jun-mediated transcription. We also found that TPA stimulates AVP gene transcription partly via the AP1 site through the activation of extracellular signal-regulated kinase (ERK) signaling. Altogether, these results suggest that a variety of Fos/Jun family member proteins stimulate the transcription of AVP gene through the AP1 site we identified. Furthermore, this effect may be activated via both PKA and PKC signaling pathways.
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