title: Vitamin D receptor overexpression in osteoblasts and osteocytes prevents bone loss during vitamin D-deficiency.
abstract: There are several lines of evidence that demonstrate the ability of 1,25-dihydroxyvitamin D (1,25(OH)2D3), acting via the vitamin D receptor (VDR) to mediate negative or positive effects in bone. Transgenic over-expression of VDR in osteoblasts and osteocytes in a mouse model (OSVDR) has been previously shown to inhibit processes of bone resorption and enhance bone formation, under conditions of adequate calcium intake. While these findings suggest that vitamin D signalling in osteoblasts and osteocytes promotes bone mineral accrual, the vitamin D requirement for this action is not well understood. In this study, 4 week old female OSVDR and wild-type (WT) mice were fed either a vitamin D-replete (1000IU/kg diet, D+) or vitamin D-deficient (D-) diet for 4 months to observe changes to bone mineral homeostasis. Tibial bone mineral volume was analysed by micro-CT and changes to bone cell activities were measured using standard dynamic histomorphometric techniques. While vitamin D-deplete WT mice demonstrated a reduction in periosteal bone accrual and overall bone mineral volume, OSVDR mice, however, displayed increased cortical and cancellous bone volume in mice which remained higher during vitamin D-depletion due to a reduced osteoclast number and increased bone formation rate. These data suggest that increased VDR-mediated activity in osteoblast and osteocytes prevents bone loss due to vitamin D-deficiency. This article is part of a Special Issue entitled '16th Vitamin D Workshop'.
authors.affiliation: School of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia.
authors.forename: Nga N
authors.initials: NN
authors.lastname: Lam
authors.affiliation: School of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia.
authors.forename: Rahma
authors.initials: R
authors.lastname: Triliana
authors.affiliation: Centre for Musculoskeletal Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, Australia.
authors.forename: Rebecca K
authors.initials: RK
authors.lastname: Sawyer
authors.affiliation: Bone Cell Biology Group, Centre for Orthopaedic & Trauma Research, The University of Adelaide, SA 5005, Australia.
authors.forename: Gerald J
authors.initials: GJ
authors.lastname: Atkins
authors.affiliation: School of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia; Centre for Musculoskeletal Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, Australia; Chemical Pathology, SA Pathology, Adelaide, South Australia, Australia.
authors.forename: Howard A
authors.initials: HA
authors.lastname: Morris
authors.affiliation: School of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia; Chemical Pathology, SA Pathology, Adelaide, South Australia, Australia.
authors.forename: Peter D
authors.initials: PD
authors.lastname: O'Loughlin
authors.affiliation: School of Health Sciences, University of Adelaide, Adelaide, South Australia, Australia; Centre for Musculoskeletal Health Research, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, Australia. Electronic address: paul.anderson@unisa.edu.au.
authors.forename: Paul H
authors.initials: PH
authors.lastname: Anderson
mesh_terms: D000818:Animals; D005260:Female; D006801:Humans; D051379:Mice; D010006:Osteoblasts / Q000378:metabolism* / Q000473:pathology; D010010:Osteoclasts / Q000378:metabolism* / Q000473:pathology; D010024:Osteoporosis / Q000378:metabolism / Q000517:prevention & control*; D018167:Receptors, Calcitriol / Q000378:metabolism*; D014808:Vitamin D Deficiency / Q000503:physiopathology*
chemical_list: D018167:Receptors, Calcitriol
keywords: Osteoblasts; Osteocytes; Transgenic mice; Vitamin D deficiency; Vitamin D receptor