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(American Journal of Pathology. 2003;162:1241-1248.)
© 2003 American Society for Investigative Pathology

Disruption of the Caveolin-1 Gene Impairs Renal Calcium Reabsorption and Leads to Hypercalciuria and Urolithiasis

Guangwen Cao*, Guang Yang*, Terry L. Timme*, Takashi Saika*, Luan D. Truong{dagger}, Takefumi Satoh*, Alexei Goltsov*, Sang Hee Park*, Taoyan Men*, Nobuyuki Kusaka*, Weihua Tian*, Chengzhen Ren*, Hongyu Wang*, Dov Kadmon*, Wei Wen Cai{ddagger}, A. Craig Chinault{ddagger}, Timothy B. Boone*, Allan Bradley{ddagger}§ and Timothy C. Thompson*¶||

From the Scott Department of Urology,* Department of Pathology,{dagger} Department of Human and Molecular Genetics,{ddagger} Department of Molecular and Cellular Biology, Department of Radiology, Baylor College of Medicine,|| Houston, Texas USA; and the The Sanger Center,§ Wellcome Trust Genome Campus, Cambridgeshire, United Kingdom

Using LoxP/Cre technology, we generated a knockout mouse homozygous for a null mutation in exon 2 of Cav1. In male Cav1-/- animals, we observed a dramatic increase in the incidence of urinary calcium stone formation. In 5-month-old male mice, the incidence of early urinary calculi was 67% in Cav1-/- mice compared to 19% in Cav1+/+ animals. Frank stone formation was observed in 13% of Cav1-/- males but was not seen in Cav1+/+ mice. Urine calcium concentration was significantly higher in Cav1-/- male mice compared to Cav1+/+ mice. In Cav1-/- mice, distal convoluted tubule cells were completely devoid of Cav1 and the localization of plasma membrane calcium ATPase was disrupted. Functional studies confirmed that active calcium absorption was significantly reduced in Cav1-/- compared to Cav1+/+ male mice. These results demonstrate that disruption of the Cav1 gene promotes the progressive steps required for urinary calcium stone formation and establish a new mouse model for urinary stone disease.




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