2001/05/16 by Rene F. Chun, Hong Chen, Lorrie Boldrick +2
paper · doi:10.1002/ajp.1016
Abstract New World primates (NWPs) have high circulating 1,25‐dihydroxyvitamin D (1,25‐(OH) 2 D) levels. Comparable levels would be harmful to Old World primates (OWPs) and humans. Thus, NWPs must have developed mechanisms of 1,25‐(OH) 2 D resistance to survive. In humans, patients with hypocalcemic vitamin D‐resistant rickets type II have high circulating vitamin D levels and vitamin D resistance due to expression of a dysfunctional vitamin D receptor (VDR). To examine if this could wholly or in part explain vitamin D resistance in NWPs, VDR from Saguinus oedipus (cotton top tamarin) NWP B95‐8 cells was cloned by reverse‐transcription polymerase chain reaction (RT‐PCR). The NWP VDR cDNA sequence showed 96% homology at the DNA level and 98% homology at the amino acid level compared to human VDR. To assay for function, NWP VDR cDNA was transiently transfected into CV‐1 cells with a vitamin D response element reporter plasmid. No difference between OWP and NWP VDR‐directed transactivation was observed. These results indicate that the mechanism of vitamin D resistance in NWPs is not due to a dysfunctional VDR, and is consistent with our hypothesis that vitamin D resistance in NWPs is mediated by overexpression of a VDR‐independent vitamin D response element binding protein. Am. J. Primatol. 54:107–118, 2001. © 2001 Wiley‐Liss, Inc.