Aberrantly expressed long noncoding RNAs in adipose-derived mesenchymal stem cells differentiation to nucleus pulposus-like cells

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Abstract

Background: Stem cells were often used for intervertebral disc degeneration (IDD) regeneration. The underlying mechanisms remain to be explored. LncRNAs were found to be related to the physiological process such as apoptosis and differentiation. Many studies focus on the messenger RNAs (mRNAs) and long non-coding RNAs (lncRNAs) between normal nucleus pulposus and degeneration nucleus pulposus. However, few studies have shed light on the different expression of lncRNA and mRNA in the differentiation. In the present study, we aimed to determine mRNAs and lncRNAs, which are differentially expressed during in human adipose-derived mesenchymal stem cells (hADSCs) differentiation process into np-like cell types and to explore the related signaling pathways and the regulatory networks. Methods: hADSCs were induced to differentiation into np-like cell under the cytokine circumstance. The mark genes of np-like cell were determined by PCR and immunology staining. Then RNA-seq was used to analysis the expression of lncRNA and mRNA in the differentiation of hADSCs into np-like cell types. The significant genes were confirmed by Gene Ontology terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway database. Results: We found 14 lncRNAs and 601 mRNAs were significantly differentially expressed in hADSCs differentiation. The RNA-seq data were confirmed by real-time PCR. Furthermore, we found Gene Ontology terms were upregulated, and downregulated and significantly enriched pathways. Moreover, gene network shows significant differentially expressed genes. Meanwhile, the relationship of significantly changed mRNAs and lncRNAs were revealed by mRNA-lncRNA co-expression network. Conclusion: Our results first explore differentially expressed lncRNAs and mRNAs in the differentiation of hADSCs into np-like cell types. These may supply useful information for better understanding of stem cell therapy and IDD regeneration.

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