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Articles in PresS, published online ahead of print March 1, 2002
Am J Physiol Renal Physiol, 10.1152/ajprenal.00357.2001
Submitted on December 7, 2001
Accepted on January 28, 2002
1 Department of Pediatrics, University of Arizona, Tucson, AZ, USA; Steele Memorial Children's Research Center, University of Arizona, Tucson, AZ, USA
2 Department of Pediatrics, University of Arizona, Tucson, AZ, USA; Department of Physiology, University of Arizona, Tucson, AZ, USA; Steele Memorial Children's Research Center, University of Arizona, Tucson, AZ, USA
3 Department of Orthopedic Surgery, University of Arizona, Tucson, AZ, USA
4 Department of Pediatrics, University of Arizona, Tucson, AZ, USA
5 Department of Pediatrics, University of Arizona, Tucson, AZ, USA; Steele Memorial Children's Research Center, University of Arizona, Tucson, AZ, USA; Department of Physiology, University of Arizona, Tucson, AZ, USA
* To whom correspondence should be addressed. E-mail: fghishan{at}peds.arizona.edu.
PHEX is a member of the neutral endopeptidase family, which is expressed predominantly on the plasma membranes of mature osteoblasts and osteocytes. While it is known that the loss of PHEX function results in X-linked hypophosphatemic rickets characterized by abnormal bone matrix mineralization and renal phosphate wasting, little is known about how PHEX is regulated. We therefore sought to determine if the murine PHEX gene is regulated by glucocorticoids, which are known to influence phosphate homeostasis and bone metabolism. Northern blot analysis revealed increased PHEX mRNA expression in glucocorticoid (GC) treated suckling mice (1.5-fold) and in rat osteogenic sarcoma (UMR-106) cells (2.5-fold). An increase was also seen in PHEX promoter activity in transiently transfected UMR-106 cells with GC treatment. Analysis of nested promoter deletions revealed that an atypical GC response element was located between bps -337 and -315. Further mutational analysis and electrophoretic mobility shift assays (EMSA) further identified bp -326 to -321 as a site involved in GC regulation. Supershift analyses and EMSA competition studies indicated that Cbf
1 transcription factor is able to bind to this region and may therefore play a role in the glucocorticoid response of the murine PHEX gene.
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