PUBLICATION
Prednisolone suppresses collagen-encoding gene expression causing cartilage defects in zebrafish larvae
- Authors
- Jiang, Y., Xin, N., Yang, J., Wu, W., Wang, M., Feng, N., Zhu, G.
- ID
- ZDB-PUB-210801-8
- Date
- 2021
- Source
- Environmental Toxicology and Pharmacology 87: 103719 (Journal)
- Registered Authors
- Keywords
- Cartilage, Glucocorticoid receptor, Glucocorticoid-induced osteoporosis, Prednisolone, Zebrafish
- MeSH Terms
-
- Animals
- Cartilage/abnormalities
- Cartilage/drug effects*
- Collagen/genetics*
- Female
- Gene Expression Regulation/drug effects*
- HEK293 Cells
- Humans
- Larva/drug effects
- Larva/genetics
- Larva/growth & development
- Male
- Prednisolone/toxicity*
- Receptors, Glucocorticoid/genetics
- Zebrafish/genetics
- Zebrafish/growth & development
- PubMed
- 34332081 Full text @ Environ. Toxicol. Pharmacol.
Citation
Jiang, Y., Xin, N., Yang, J., Wu, W., Wang, M., Feng, N., Zhu, G. (2021) Prednisolone suppresses collagen-encoding gene expression causing cartilage defects in zebrafish larvae. Environmental Toxicology and Pharmacology. 87:103719.
Abstract
Glucocorticoid-induced osteoporosis (GIOP) is a clinically important disease. Despite many studies, the intrinsic pathogenesis of GIOP is still not fully understood. Cartilage is the target tissue of the glucocorticoid prednisolone (PN). To explore the intrinsic mechanism of PN-induced cartilage damage, we performed cartilage staining and cell transfection experiments in zebrafish larvae treated with PN. The results showed that PN caused cartilage damage in zebrafish at 25 μM. Moreover, after treatment with PN, it was found that collagen-encoding gene expression was significantly reduced. Further research revealed that the glucocorticoid receptor (GR) mediates the transcriptional inhibition of collagen genes by PN. These results indicate that glucocorticoids cause cartilage damage by inhibiting the expression of collagen genes through their receptors. Our study provides new insights into GIOP.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping