Vitamin D receptor in chondrocytes promotes osteoclastogenesis and regulates FGF23 production in osteoblasts
J. Clin. Invest. Ritsuko Masuyama, et al. 116:3150 doi:10.1172/JCI29463 [Go to this article.]

Figure 1
Inactivation of the VDR gene in chondrocytes. (A) Schematic representation of targeting construct pNT vector/VDR, the VDR^WT allele, and the VDR^fl allele after Cre excision of the floxed neo cassette and probe used for identifying correct Cre excision of floxed exon 2. Restriction sites are indicated. Ex, exon. (B) Southern blot of SacI-digested genomic DNA from Cre^–VDR^fl/fl and Cre⁺VDR^fl/fl mice using internal probe. (C) VDR gene expression in growth-plate chondrocytes of Cre^–VDR^fl/fl (Cre^–) and Cre⁺VDR^fl/fl (Cre⁺) mice (n = 6) was assessed by qRT-PCR analysis and calculated as a ratio to the HPRT mRNA copies. Cre^–VDR^fl/fl value was set at 100%. **P < 0.01 versus Cre^–VDR^fl/fl. (D) qRT-PCR analysis of CYP24 mRNA levels in primary chondrocyte culture stimulated with vehicle (veh) or 1,25(OH)₂D₃ (10^–10 M and 10^–8 M) for 48 hours and 72 hours. Values are corrected for HPRT mRNA copies and are shown as means ± SEM in log scale. **P < 0.01 versus vehicle.