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Am J Physiol Cell Physiol 273: C1562-C1570, 1997;
0363-6143/97 $5.00
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Vol. 273, Issue 5, C1562-C1570, November 1997

Aqp1 expression in erythroleukemia cells: genetic regulation of glucocorticoid and chemical induction

Chulso Moon1,2, Landon S. King2,3, and Peter Agre1,2

1 Department of Biological Chemistry, 2 Department of Medicine, and 3 Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205-2185

The aquaporin-1 (AQP1) water channel protein is expressed in multiple mammalian tissues by several different developmental programs; however, the genetic regulation is undefined. The proximal promoter of mouse Aqp1 contains multiple putative cis-acting regulatory elements, and mouse erythroleukemia (MEL) cells are a well-characterized model for erythroid differentiation. Corticosteroid or dimethyl sulfoxide (DMSO) exposure induces AQP1 protein expression in MEL cells, and transcriptional regulation was investigated by transient transfections with Aqp1 promoter-reporter constructs. Dexamethasone induction is abrogated by deletion of two glucocorticoid response elements -0.5 kilobases (kb) from the transcription initiation site. Mutation of the GATA element at -0.62 kb has no effect, whereas mutation of the CACCC site at -37 bp significantly reduces DMSO-induced promoter activity. Hydroxyurea induces expression of AQP1 protein without acting through the proximal promoter. The MEL cell line is a reproducible erythroid model system for studying transcriptional regulation of the Aqp1 gene while determining the consequences on AQP1 protein biosynthesis.

transcriptional regulation; water channels; erythroid tissue; promoter; protein biosynthesis; aquaporin-1


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