A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
WNT16 overexpression partly protects against glucocorticoid-induced bone loss
Tekijät: Claes Ohlsson, Karin H. Nilsson, Petra Henning, Jianyao Wu, Karin L. Gustafsson, Matti Poutanen, Ulf H. Lerner, Sofia Movérare-Skrtic
Julkaisuvuosi: 2018
Journal: American Journal of Physiology : Endocrinology and Metabolism
Tietokannassa oleva lehden nimi: American journal of physiology. Endocrinology and metabolism
Lehden akronyymi: Am J Physiol Endocrinol Metab
Vuosikerta: 314
Numero: 6
Aloitussivu: E597
Lopetussivu: E604
Sivujen määrä: 8
ISSN: 1522-1555
DOI: https://doi.org/10.1152/ajpendo.00292.2017
Tiivistelmä
) or vehicle for 4 wk. We first observed that GC treatment decreased the Wnt16 mRNA levels in bone of female mice (-56.4 ± 6.1% compared with vehicle, P < 0.001). We next evaluated if WNT16 overexpression protects against GC-induced bone loss. Dual-energy X-ray absorptiometry analyses revealed that GC treatment decreased total body bone mineral density in WT mice (-3.9 ± 1.2%, P = 0.028) but not in Obl-Wnt16 mice (+1.3 ± 1.4%, nonsignificant). Microcomputed tomography analyses showed that GC treatment decreased trabecular bone volume fraction (BV/TV) of the femur in WT mice ( P = 0.019) but not in Obl-Wnt16 mice. Serum levels of the bone formation marker procollagen type I N-terminal propeptide were substantially reduced by GC treatment in WT mice (-50.3 ± 7.0%, P = 0.008) but not in Obl-Wnt16 mice (-3.8 ± 21.2%, nonsignificant). However, the cortical bone thickness in femur was reduced by GC treatment in both WT mice and Obl-Wnt16 mice. In conclusion, GC treatment decreases Wnt16 mRNA levels in bone and WNT16 overexpression partly protects against GC-induced bone loss.
) or vehicle for 4 wk. We first observed that GC treatment decreased the Wnt16 mRNA levels in bone of female mice (-56.4 ± 6.1% compared with vehicle, P < 0.001). We next evaluated if WNT16 overexpression protects against GC-induced bone loss. Dual-energy X-ray absorptiometry analyses revealed that GC treatment decreased total body bone mineral density in WT mice (-3.9 ± 1.2%, P = 0.028) but not in Obl-Wnt16 mice (+1.3 ± 1.4%, nonsignificant). Microcomputed tomography analyses showed that GC treatment decreased trabecular bone volume fraction (BV/TV) of the femur in WT mice ( P = 0.019) but not in Obl-Wnt16 mice. Serum levels of the bone formation marker procollagen type I N-terminal propeptide were substantially reduced by GC treatment in WT mice (-50.3 ± 7.0%, P = 0.008) but not in Obl-Wnt16 mice (-3.8 ± 21.2%, nonsignificant). However, the cortical bone thickness in femur was reduced by GC treatment in both WT mice and Obl-Wnt16 mice. In conclusion, GC treatment decreases Wnt16 mRNA levels in bone and WNT16 overexpression partly protects against GC-induced bone loss.
Turun yliopiston Tutkimustietojärjestelmän portaali