High-throughput sequencing analyses of transcript changes in growth plates upon dexamethasone treatment

Glucocorticoid-induced growth retardation (GIGR) is a common adverse effect of glucocorticoid treatment in pediatric patients. Accumulating evidence indicates that non-coding RNAs (ncRNAs) are involved in the pathogenesis of GIGR, but the roles of specific ncRNAs in growth remain largely unknown. In this study, we established an in vivo GIGR rat model by 7- or 14- day dexamethasone (Dex) treatment and performed high-throughput RNA sequencing to identify mRNAs, lncRNAs, circRNAs, and miRNAs differentially expressed in GIGR rats relative to control rats in the growth plates.High-throughput RNA sequencing identified 1718 mRNAs, 896 lncRNAs, 60 circRNAs, and 72 miRNAs with differing expression levels at 7d group. At 14d group, 1515 mRNAs, 880 lncRNAs, 46 circRNAs, and 55 miRNAs with differential expression were identified. Eight mRNAs were validated by RT-qPCR, with expression level differences consistent with RNA sequencing data. Function enrichment analyses indicate that the PI3K-Akt signaling pathway, NF-kappa B signaling pathway, and TGF-beta signaling pathway participated in the development of the GIGR. Then, ceRNA networks were constructed to investigate the potential molecular mechanisms of ncRNAs. These results provide new insights for exploring the molecular mechanisms underlying GIGR. Overall design: mRNA, lncRNA,circRNA and miRNA profiles of growth plate chondrocytes from GIGR rats and control rats