Abstract
Background Intervertebral disc degeneration (IDD) disease is a global challenge because of its predominant pathogenic factor in triggering low back pain, whereas cartilaginous endplate degeneration (CEPD) is the main cause of IDD. Accumulating evidence have indicated that the differentially expressed microRNAs (DEMs) and differentially expressed genes (DEGs) have been determined to be involved in multiple biological processes to mediate CEPD progression. However, the differentially expressed circular RNAs (DECs) and their potential biofunctions in CEPD have not been identified. Methods GSE153761 dataset was analyzed using R software to predict DECs, DEMs, and DEGs. Pathway enrichment analysis of DEGs and host genes of DECs and protein-protein interaction network of DEGs were conducted to explore their potential biofunctions. Furthermore, we explore the potential relationship between DEGs and DECs. Results There were 74 DECs, 17 DEMs, and 68 DEGs upregulated whereas 50 DECs, 16 DEMs, and 67 DEGs downregulated in CEPD group. Pathway analysis unveiled that these RNAs might regulate CEPD via mediating inflammatory response, ECM metabolism, chondrocytes apoptosis, and chondrocytes growth. A total of 17 overlapping genes were predicted between the host genes of DEGs and DECs, such as SDC1 and MAOA. Moreover, 6 upregulated DECs, of which hsa_circ_0052830 was the most upregulated circRNA in CEPD, were derived from the host genes SDC1, whereas 8 downregulated DECs were derived from the host genes MAOA. Conclusion This will provide novel clues for future experimental studies to elucidate the pathomechanism of CEPD and therapeutic targets for CEPD-related diseases.
Highlights
Intervertebral disc degeneration (IDD) diseases are a global challenge that contributed to dyskinesia in patients and the increased of socioeconomic burden [1,2,3]
During IDD, the water in nucleus pulposus (NP) tissue continually decreases, causing the pyknotic substances deposited in the cartilaginous endplates (CEP) and gradually calcifies, the calcified CEP leads to the decrease of CEP permeability [8].CEP degeneration (CEPD) caused by endplate chondrocyte death and calcification can block this exchange channel, which further aggravates IDD and the failure of endogenous repair, and forms a vicious cycle [9, 10]
Compared with the expression of circRNAs, miRNAs, and genes in the normal CEP group, a volcano plot reflected that there were 74 differentially expressed circular RNAs (DECs), 17 differentially expressed microRNAs (DEMs), and 68 differentially expressed genes (DEGs) upregulated whereas 50 DECs, 16 DEMs, and 67 DEGs downregulated in cartilaginous endplate degeneration (CEPD) group with the screening criteria of ∣log2 ðfold − changeÞ ∣ >2 and p value < 0.05 (Figures 1(b)–1(d), Supplementary Table 2)
Summary
Intervertebral disc degeneration (IDD) diseases are a global challenge that contributed to dyskinesia in patients and the increased of socioeconomic burden [1,2,3]. Intervertebral disc degeneration (IDD) disease is a global challenge because of its predominant pathogenic factor in triggering low back pain, whereas cartilaginous endplate degeneration (CEPD) is the main cause of IDD. GSE153761 dataset was analyzed using R software to predict DECs, DEMs, and DEGs. Pathway enrichment analysis of DEGs and host genes of DECs and protein-protein interaction network of DEGs were conducted to explore their potential biofunctions. A total of 17 overlapping genes were predicted between the host genes of DEGs and DECs, such as SDC1 and MAOA. This will provide novel clues for future experimental studies to elucidate the pathomechanism of CEPD and therapeutic targets for CEPD-related diseases
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
