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Proc. Natl. Acad. Sci. USA
Vol. 94, pp. 9831-9835, September 1997
Medical Sciences

Targeted ablation of the vitamin D receptor: An animal model of vitamin D-dependent rickets type II with alopecia

Yan Chun Li*, Alison E. Pirro*, Michael Amlingdagger ,Dagger , Gunter DellingDagger , Roland Barondagger , Roderick Bronson§, and Marie B. Demay*,

* Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, 15 Fruit Street, Boston, MA 02114; dagger  Department of Cell Biology, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06510; Dagger  Department of Bone Pathology, Hamburg University School of Medicine, Martinistrasse 52, 20246 Hamburg, Germany; and § Tufts University School of Veterinary Medicine and Human Nutrition Research Center, 711 Washington Street, Boston, MA 02111

Edited by Bert W. O'Malley, Baylor College of Medicine, Houston, TX, and approved July 1, 1997 (received for review May 15, 1997)

Vitamin D, the major steroid hormone that controls mineral ion homeostasis, exerts its actions through the vitamin D receptor (VDR). The VDR is expressed in many tissues, including several tissues not thought to play a role in mineral metabolism. Studies in kindreds with VDR mutations (vitamin D-dependent rickets type II, VDDR II) have demonstrated hypocalcemia, hyperparathyroidism, rickets, and osteomalacia. Alopecia, which is not a feature of vitamin D deficiency, is seen in some kindreds. We have generated a mouse model of VDDR II by targeted ablation of the second zinc finger of the VDR DNA-binding domain. Despite known expression of the VDR in fetal life, homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months. They become hypocalcemic at 21 days of age, at which time their parathyroid hormone (PTH) levels begin to rise. Hyperparathyroidism is accompanied by an increase in the size of the parathyroid gland as well as an increase in PTH mRNA levels. Rickets and osteomalacia are seen by day 35; however, as early as day 15, there is an expansion in the zone of hypertrophic chondrocytes in the growth plate. In contrast to animals made vitamin D deficient by dietary means, and like some patients with VDDR II, these mice develop progressive alopecia from the age of 4 weeks.


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