Does the specific deletion of VDR in mature osteoblasts and osteocytes impair skeletal health?
To extend our understanding of the role of vitamin D activity within osteoblasts/osteocytes on bone homeostasis we will generate and extensively characterise a mouse model in which the VDR has been specifically deleted in terminally differentiated mineralizing osteoblasts and osteocytes (OBL-VDRKOs) using Cre/loxP technology. OBL-VDRKOs will be generated using two mouse lines; A) a transgenic mouse line in which Cre (a site specific recombinase) is expressed specifically in mineralizing osteoblasts and osteocytes (osteocalcin-Cre mice (Osteoblast-specific knockout of the insulin-like growth factor (IGF) receptor gene reveals an essential role of IGF signalling in bone matrix mineralization; B) a mouse line in which exon 2 of the VDR is flanked by loxP sites (VDR-loxP mice). Breeding of the osteocalcin-Cre mouse line (A) with the VDR-loxP mouse line (B) results in a mouse line in which the VDR is inactivated specifically in mineralizing osteoblasts and osteocytes (OBL-VDRKOs).We have su
