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Physiol. Genomics (March 18, 2008). doi:10.1152/physiolgenomics.00024.2008
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Submitted on January 28, 2008
Accepted on March 13, 2008

Transcriptional Adaptation to Clcn5 Knockout in Proximal Tubules of the Mouse Kidney

Jerry Wright1, Marcelo M. Morales2, Jackson Sousa-Menzes2, Debora Ornellas2, Jennifer Sipes3, and Sandra E. Guggino4*

1 Physiology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
2 Instituto de Biophysica Carlos Chagas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
3 Gastrointestinal Division, Johns Hopkins University School of Medicine, Ross Building, Room 929, Baltimore,, Maryland, 21205, United States
4 Gastrointestinal Division and Department of Physiology, Johns Hopkins University School of Medicine, Baltimore,, Maryland, United States

* To whom correspondence should be addressed. E-mail: sguggino{at}jhmi.edu.

Dent disease has multiple defects attributed to proximal tubule malfunction including low molecular weight proteinuria, aminoaciduria, phosphaturia and glycosuria. In order to understand the changes in kidney function of the Clc5 transporter gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal tubules of mouse kidneys. We found many changes in gene expression not known previously to be altered in this disease. Genes involved in lipid metabolism, organ development and organismal physiological processes had the greatest number of significantly changed transcripts. In addition, genes of catalytic activity and transporter activity also had a great number of changed transcripts. Overall 720 genes are expressed differentially in the proximal tubules of the Dent Clcn5 knockout mouse model compared to those of control wild type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease.






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