A mutation in the mouse Chd2 chromatin remodeling enzyme results in a complex renal phenotype
Authors
Marfella, Concetta G. A.Henninger, Nils
LeBlanc, Scott E.
Krishnan, Namrata
Garlick, David S.
Holzman, Lawrence B.
Imbalzano, Anthony N.
UMass Chan Affiliations
Department of Internal Medicine, Division of Renal MedicineDepartment of Cancer Biology
Department of Neurology
Department of Cell Biology
Document Type
Journal ArticlePublication Date
2008-12-15Keywords
Animals*Chromatin Assembly and Disassembly
DNA-Binding Proteins
Epigenesis, Genetic
Glomerulonephritis, Membranous
Kidney
Kidney Diseases
Mice
*Mutation
Phenotype
Proteinuria
Cell Biology
Life Sciences
Medicine and Health Sciences
Nephrology
Metadata
Show full item recordAbstract
BACKGROUND AND AIMS: Glomerular diseases are the third leading cause of kidney failure worldwide, behind only diabetes and hypertension. The molecular mechanisms underlying the cause of glomerular diseases are still largely unknown. The identification and characterization of new molecules associated with glomerular function should provide new insights into understanding the diverse group of glomerular diseases. The Chd2 protein belongs to a family of enzymes involved in ATP-dependent chromatin remodeling, suggesting that it likely functions as an epigenetic regulator of gene expression via the modification of chromatin structure. METHODS: In this study, we present a detailed histomorphologic characterization of mice containing a mutation in the chromodomain helicase DNA-binding protein 2 (Chd2). RESULTS: We show that Chd2-mutant mice present with glomerulopathy, proteinuria, and significantly impaired kidney function. Additionally, serum analysis revealed decreased hemoglobin and hematocrit levels in Chd2-mutant mice, suggesting that the glomerulopathy observed in these mice is associated with anemia. CONCLUSION: Collectively, the data suggest a role for the Chd2 protein in the maintenance of kidney function.Source
Kidney Blood Press Res. 2008;31(6):421-32. Link to article on publisher's siteDOI
10.1159/000190788Permanent Link to this Item
http://hdl.handle.net/20.500.14038/39374PubMed ID
19142019Related Resources
Link to Article in PubMedae974a485f413a2113503eed53cd6c53
10.1159/000190788