PUBLICATION

Possible mechanisms of prednisolone-induced osteoporosis in zebrafish larva

Authors
He, H., Wang, C., Tang, Q., Yang, F., Xu, Y.
ID
ZDB-PUB-180418-12
Date
2018
Source
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie   101: 981-987 (Journal)
Registered Authors
Yang, Fan
Keywords
ECM, GIOP, Osteoblast, Osteoclast
MeSH Terms
  • Animals
  • Extracellular Matrix/genetics
  • Extracellular Matrix/metabolism
  • Gene Expression Regulation/drug effects
  • Larva/drug effects
  • Osteoblasts/drug effects
  • Osteoblasts/metabolism
  • Osteoporosis/chemically induced*
  • Osteoporosis/pathology*
  • Phenotype
  • Prednisolone/adverse effects*
  • Zebrafish/metabolism*
PubMed
29635908 Full text @ Biomed. Pharmacother.
Abstract
Glucocorticoid-induced osteoporosis (GIOP) is a serious clinical bone disease that results from the long-term consumption of glucocorticoids or glucocorticoid-like drugs. Although many studies have attempted to determine the mechanisms of GIOP, they are still unclear. In this study, we established a zebrafish model of glucocorticoid-like drug-induced osteoporosis by treating larvae with prednisolone. We then quantified the expression of a selection of extracellular matrix (ECM)-, osteoblast-, and osteoclast-related genes. Our results showed that at 15 days post fertilization, zebrafish larvae treated with 25 μM prednisolone are a suitable model for GIOP, not only owing to the decrease in robust bone mass but also because of significant alterations in gene expression. The quantification of the expression of ECM-, osteoblast-, and osteoclast- related genes revealed that mmp9 and mmp13 were significantly upregulated and entpd5a, acp5a, and sost were significantly downregulated. These genes may be a target for future research into GIOP. Our study thus provides new insights into GIOP.
Genes / Markers
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping