Data from: Prednisolone induces osteoporosis-like phenotypes via focal adhesion signaling pathway in zebrafish larvae

Patients taking glucocorticoid or glucocorticoid-like drugs for an extended period of time may develop osteoporosis, termed glucocorticoid-induced osteoporosis (GIOP). GIOP is the most common form of secondary osteoporosis, but the mechanism underlying its development is unclear. In the present study, we used prednisolone to treat zebrafish larvae to investigate GIOP. Our RNA deep-sequencing (RNA-seq) results show that prednisolone affects genes known to act in the extracellular region. Therefore the extracellular region, extracellular matrix, and collagen trimer might be involved in glucocorticoid-induced osteoporosis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that the focal adhesion signaling pathway is the most enriched signaling pathway in terms of differentially expressed genes (DEGs). In this pathway, two adapter proteins, itga10 and itgbl1, were down-regulated in the prednisolone-treated larvae. Further experiments showed that prednisolone contributes to GIOP by down-regulating itga10 and itgbl1.

长期服用糖皮质激素或类糖皮质激素药物的患者可能会罹患骨质疏松，该病症被称为糖皮质激素诱导性骨质疏松（glucocorticoid-induced osteoporosis, GIOP）。GIOP是最常见的继发性骨质疏松类型，但其发病机制尚未明确。在本研究中，我们通过泼尼松龙处理斑马鱼幼体以探究GIOP的发病机制。我们的RNA深度测序（RNA-seq）结果显示，泼尼松龙会影响已知在细胞外区域发挥功能的基因。因此，细胞外区域、细胞外基质及胶原三聚体可能参与了糖皮质激素诱导性骨质疏松的发生。京都基因与基因组百科全书（KEGG）通路分析表明，在差异表达基因（DEGs）中，黏着斑信号通路是富集程度最高的信号通路。在该通路中，两种衔接蛋白itga10与itgbl1在泼尼松龙处理的幼体内表达量下调。进一步实验证实，泼尼松龙通过下调itga10与itgbl1的表达，进而引发GIOP。