Transcriptional adaptation to Clcn5 knockout in proximal tubules of mouse kidney

Jerry Wright; Marcelo M. Morales; Jackson Sousa-Menzes; Debora Ornellas; Jennifer Sipes; Yan Cui; Isabelle Cui; Phuson Hulamm; Valeriu Cebotaru; Liudmila Cebotaru; William B. Guggino; Sandra E. Guggino

doi:10.1152/physiolgenomics.00024.2008

Transcriptional adaptation to Clcn5 knockout in proximal tubules of mouse kidney

Jerry Wright, Marcelo M. Morales, Jackson Sousa-Menzes, Debora Ornellas, Jennifer Sipes, Yan Cui, Isabelle Cui, Phuson Hulamm, Valeriu Cebotaru, Liudmila Cebotaru, William B. Guggino, Sandra E. Guggino

Research output: Contribution to journal › Article › peer-review

27 Scopus citations

Abstract

Dent disease has multiple defects attributed to proximal tubule malfunction including low-molecular-weight proteinuria, aminoaciduria, phosphaturia, and glycosuria. To understand the changes in kidney function of the Clc5 chloride/proton exchanger gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal S1 and S2 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 with those of control wild-type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease.

Original language	English (US)
Pages (from-to)	341-354
Number of pages	14
Journal	Physiological Genomics
Volume	33
Issue number	3
DOIs	https://doi.org/10.1152/physiolgenomics.00024.2008
State	Published - May 1 2008
Externally published	Yes

Keywords

Cholesterol
Dent disease
Endocytosis
Gene array

ASJC Scopus subject areas

Physiology
Genetics

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10.1152/physiolgenomics.00024.2008

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title = "Transcriptional adaptation to Clcn5 knockout in proximal tubules of mouse kidney",

abstract = "Dent disease has multiple defects attributed to proximal tubule malfunction including low-molecular-weight proteinuria, aminoaciduria, phosphaturia, and glycosuria. To understand the changes in kidney function of the Clc5 chloride/proton exchanger gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal S1 and S2 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 with those of control wild-type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease.",

keywords = "Cholesterol, Dent disease, Endocytosis, Gene array",

author = "Jerry Wright and Morales, {Marcelo M.} and Jackson Sousa-Menzes and Debora Ornellas and Jennifer Sipes and Yan Cui and Isabelle Cui and Phuson Hulamm and Valeriu Cebotaru and Liudmila Cebotaru and Guggino, {William B.} and Guggino, {Sandra E.}",

year = "2008",

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doi = "10.1152/physiolgenomics.00024.2008",

language = "English (US)",

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AU - Wright, Jerry

AU - Morales, Marcelo M.

AU - Sousa-Menzes, Jackson

AU - Ornellas, Debora

AU - Sipes, Jennifer

AU - Cui, Yan

AU - Cui, Isabelle

AU - Hulamm, Phuson

AU - Cebotaru, Valeriu

AU - Cebotaru, Liudmila

AU - Guggino, William B.

AU - Guggino, Sandra E.

PY - 2008/5/1

Y1 - 2008/5/1

N2 - Dent disease has multiple defects attributed to proximal tubule malfunction including low-molecular-weight proteinuria, aminoaciduria, phosphaturia, and glycosuria. To understand the changes in kidney function of the Clc5 chloride/proton exchanger gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal S1 and S2 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 with those of control wild-type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease.

AB - Dent disease has multiple defects attributed to proximal tubule malfunction including low-molecular-weight proteinuria, aminoaciduria, phosphaturia, and glycosuria. To understand the changes in kidney function of the Clc5 chloride/proton exchanger gene knockout mouse model of Dent disease, we examined gene expression profiles from proximal S1 and S2 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 with those of control wild-type mice. The fingerprint of these gene changes may help us to understand the phenotype of Dent disease.

KW - Cholesterol

KW - Dent disease

KW - Endocytosis

KW - Gene array

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Transcriptional adaptation to Clcn5 knockout in proximal tubules of mouse kidney

Abstract

Keywords

ASJC Scopus subject areas

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