Prednisolone induces osteoporosis-like phenotype in regenerating zebrafish scales

  title={Prednisolone induces osteoporosis-like phenotype in regenerating zebrafish scales},
  author={Erik de Vrieze and M. A. H. J. van Kessel and H. M. Peters and F. A. Tom Spanings and Gert Flik and Juriaan R. Metz},
  journal={Osteoporosis International},
SummaryWe demonstrate that glucocorticoids induce an osteoporotic phenotype in regenerating scales of zebrafish. Exposure to prednisolone results in altered mineral content, enhanced matrix breakdown, and an osteoporotic gene-expression profile in osteoblasts and osteoclasts. This highlights that the zebrafish scale provides a powerful tool for preclinical osteoporosis research.IntroductionThis study aims to evaluate whether glucocorticoid (prednisolone) treatment of zebrafish induces an… 
Alendronate rescued osteoporotic phenotype in a model of glucocorticoid‐induced osteoporosis in adult zebrafish scale
The treatment with PN in association with alendronate has surprisingly resulted in a significant decrease of TRAP activity and increase of ALP compared to PN‐treated fish in biochemical and histological assays confirming the action of alendronsate against GIOP in fish as well in humans.
Evaluation of Dexamethasone-Induced Osteoporosis In Vivo Using Zebrafish Scales
A rapid dexamethasone-induced osteoporosis animal model and enzyme assay method that could help to design better treatments for GIOP are shown and a method to measure the activities of cathepsin K, TRAP, and ALP using zebrafish scales is developed.
Possible mechanisms of prednisolone-induced osteoporosis in zebrafish larva.
Influence of Prednisolone and Alendronate on the de novo Mineralization of Zebrafish Caudal Fin
As an emerging model of osteoporosis, regrowth of zebrafish caudal fin was shown to be a reliable assay system to investigate the various effects of medicines in the de novo mineralization process.
Immune Suppressive and Bone Inhibitory Effects of Prednisolone in Growing and Regenerating Zebrafish Tissues
  • K. Geurtzen, A. Vernet, F. Knopf
  • Biology, Medicine
    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research
  • 2017
It is shown that treatment with the glucocorticoid prednisolone impacts on the number, activity and differentiation of osteoblasts, osteoclasts, and immune cells during ontogenetic growth, homeostasis, and regeneration of zebrafish bone.
Age-dependent modulation of bone metabolism in zebrafish scales as new model of male osteoporosis in lower vertebrates
The early bone aging mechanisms in male zebrafish scales are investigated evaluating the physiological changes and the effects of prednisolone, a pro-osteoporotic drug to identify the early mechanisms of bone aging and new therapeutic strategies to prevent age-related bone alterations in humans.
Prednisolone induces osteoporosis-like phenotypes via focal adhesion signaling pathway in zebrafish larvae
RNA deep-sequencing results show that prednisolone affects genes known to act in the extracellular region, and glucocorticoid-induced osteoporosis, and focal adhesion signaling pathway genes (itga10 and itgbl1) might be involved in GIOP.
Hydroxysafflor Yellow A Promoted Bone Mineralization and Inhibited Bone Resorption Which Reversed Glucocorticoids-Induced Osteoporosis
HYA had the potential to prevent and heal GCIOP by promoting bone mineralization, osteoblasts viability, and bone collagen expression and inhibiting bone resorption.
Regenerating zebrafish scales express a subset of evolutionary conserved genes involved in human skeletal disease
Scales have a strong osteogenic expression profile comparable to other elements of the dermal skeleton, enriched in genes that favour collagen matrix growth, and are shown to express an evolutionarily conserved sub-population of genes that are relevant to human skeletal disease.


Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
Evidence is provided that glucocorticoid-induced bone disease arises from changes in the numbers of bone cells, whereas decreased production and apoptosis of osteoblasts would account for the decline in bone formation and trabecular width.
Glucocorticoid excess in mice results in early activation of osteoclastogenesis and adipogenesis and prolonged suppression of osteogenesis: a longitudinal study of gene expression in bone tissue from glucocorticoid-treated mice.
Novel interventions with agents that modulate either Wnt signaling or mineralization may be effective in GC-induced osteoporosis.
Prevention of glucocorticoid-induced bone loss in mice by inhibition of RANKL.
It is indicated that RANKL inhibition by denosumab prevents glucocorticoid-induced loss of bone mass and strength in hRANKL-knockin mice.
Osteoblast and osteoclast behavior in zebrafish cultured scales
Zebrafish scales cultured until 72 h can be considered as an innovative model of explanted organ culture to assay the ability of chemical compounds to modulate the metabolism of bone cells.
Osteoblastic activity and estrogenic response in the regenerating scale of goldfish, a good model of osteogenesis.
Stimulation of osteoprotegerin ligand and inhibition of osteoprotegerin production by glucocorticoids in human osteoblastic lineage cells: potential paracrine mechanisms of glucocorticoid-induced osteoporosis.
The hypothesis that glucocorticoids promote osteoclastogenesis by inhibiting OPG and concurrently stimulating OPG-L production by osteoblastic lineage cells, thereby enhancing bone resorption is supported.
The OPG/RANKL/RANK system in metabolic bone diseases.
The capacity for OPG to antagonize the increases in bone loss seen in many rodent models of metabolic bone disease implicates RANKL/OPG imbalances as the likely etiology and supports the potential role for a RankL antagonist as a therapeutic intervention in these settings.
Features of mono‐ and multinucleated bone resorbing cells of the zebrafish Danio rerio and their contribution to skeletal development, remodeling, and growth
Bone resorption is primarily subjected to the demands of growth, the appearance of mono‐ and multinucleated osteoclasts is site‐ and age‐related, and bone remodeling occurs.