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J. Biol. Chem., Vol. 282, Issue 20, 14923-14931, May 18, 2007

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Thyroid Transcription Factor-1 Facilitates Cerebrospinal Fluid Formation by Regulating Aquaporin-1 Synthesis in the Brain^*

Jae Geun Kim¹, Young June Son¹, Chang Ho Yun¹, Young Il Kim, Il Seong Nam-goong, Jun Heon Park², Sang Kyu Park^¶, Sergio R. Ojeda^||3, Angela Valentina D'Elia^**4, Giuseppe Damante^**4, and Byung Ju Lee⁵

From the Department of Biological Sciences, College of Natural Sciences, University of Ulsan, Ulsan 680-749, South Korea, the Department of Internal Medicine and ^¶Department of Pediatrics, Ulsan University Hospital, Ulsan 682-060, South Korea, the ^||Division of Neuroscience, Oregon National Primate Research Center/Oregon Health and Science University, Beaverton, Oregon 97006, and the ^**Department of Biomedical Sciences and Technologies, University of Udine, 33100 Udine, Italy

In the brain, aquaporin-1 (AQP-1), a water channel for high osmotic water permeability, is mainly expressed in the apical membrane of the ventricular choroid plexus and regulates formation of cerebrospinal fluid (CSF). Although the physiology of AQP-1 has been the subject of several publications, much less is known about the trans-acting factors involved in the control of AQP-1 gene expression. Here we report that TTF-1, a homeodomain-containing transcriptional regulator, is coexpressed with AQP-1 in the rat brain choroid plexus and enhances AQP-1 gene transcription by binding to conserved core TTF-1-binding motifs in the 5'-flanking region of the AQP-1 gene. Intracerebroventricular administration of an antisense TTF-1 oligodeoxynucleotide significantly decreased AQP-1 synthesis and reduced CSF formation. In addition, blockade of TTF-1 synthesis increased survival of the animals following acute water intoxication-induced brain edema. These results suggest that TTF-1 is physiologically involved in the transcriptional control of AQP-1, which is required for CSF formation.

Received for publication, February 16, 2007 , and in revised form, March 19, 2007.

^* This work was supported in part by Korea Research Foundation Grant KRF-2002-015-CS0045. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Supported in part by Neurobiological Research Fund B020203 and Brain Korea 21 grant.

² Worked as a volunteer for this study. Present address: University of Washington, Seattle, WA 98105.

³ Supported by National Institutes of Health Grants HD25123, RR00163, and U54 HD18185 through cooperative agreement as part of the Specialized Cooperative Center Program in Reproduction Research.

⁴ Supported by a Cofinanziamento Progetti di Ricerca di Rilevante Interesse Nazionale from Ministero dell'Università e della Ricerca.

⁵ To whom correspondence should be addressed. Tel.: 82-52-259-2351; Fax: 82-52-259-1694; E-mail: bjlee{at}ulsan.ac.kr.

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