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Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1

BACKGROUND: Gene regulatory network analysis has found that long noncoding ribonucleic acids (lncRNAs) are strongly associated with the pathogenesis of osteoarthritis. OBJECTIVES: To determine the differential expression of lncRNAs and microRNAs (miRNAs) in normal chondrocytes and those from a model...

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Autores principales: Wang, Guoliang, He, Lu, Xiang, Yaoyu, Jia, Di, Li, Yanlin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Sciendo 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10321185/
https://www.ncbi.nlm.nih.gov/pubmed/37551168
http://dx.doi.org/10.2478/abm-2022-0021
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author Wang, Guoliang
He, Lu
Xiang, Yaoyu
Jia, Di
Li, Yanlin
author_facet Wang, Guoliang
He, Lu
Xiang, Yaoyu
Jia, Di
Li, Yanlin
author_sort Wang, Guoliang
collection PubMed
description BACKGROUND: Gene regulatory network analysis has found that long noncoding ribonucleic acids (lncRNAs) are strongly associated with the pathogenesis of osteoarthritis. OBJECTIVES: To determine the differential expression of lncRNAs and microRNAs (miRNAs) in normal chondrocytes and those from a model of articular chondrocyte degeneration. METHODS: Chondrocytes were cultured from cartilage obtained from patients diagnosed with osteoarthritis of the knee. Stromal cell-derived factor-1 (SDF-1) was used to induce their degeneration. Total RNA was extracted, analyzed, amplified, labeled, and hybridized on a chip to determine expression. The set of enriched differentially expressed miRNAs was analyzed by gene ontology and the Kyoto Encyclopedia of Genes and Genomes to describe the functional properties of the key biological processes and pathways. We conducted a bioinformatics analysis using Cytoscape to elucidate the interactions between miRNAs and proteins. RESULTS: We found that the expression of 186 lncRNAs was significantly different in the model of chondrocyte degeneration, in which 88 lncRNAs were upregulated, and 98 were downregulated. Expression of 684 miRNAs was significantly different. Analysis of the protein–protein interaction (PPI) network indicated that the genes for CXCL10, ISG15, MYC, MX1, OASL, IFIT1, RSAD2, MX2, IFI44L, and BST2 are the top 10 core genes, identifying the most important functional modules to elucidate the differential expression of miRNAs. CONCLUSIONS: These data may provide new insights into the molecular mechanisms of chondrocyte degeneration in osteoarthritis, and the identification of lncRNAs and miRNAs may provide potential targets for the differential diagnosis and therapy of osteoarthritis.
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spelling pubmed-103211852023-08-07 Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1 Wang, Guoliang He, Lu Xiang, Yaoyu Jia, Di Li, Yanlin Asian Biomed (Res Rev News) Original Article BACKGROUND: Gene regulatory network analysis has found that long noncoding ribonucleic acids (lncRNAs) are strongly associated with the pathogenesis of osteoarthritis. OBJECTIVES: To determine the differential expression of lncRNAs and microRNAs (miRNAs) in normal chondrocytes and those from a model of articular chondrocyte degeneration. METHODS: Chondrocytes were cultured from cartilage obtained from patients diagnosed with osteoarthritis of the knee. Stromal cell-derived factor-1 (SDF-1) was used to induce their degeneration. Total RNA was extracted, analyzed, amplified, labeled, and hybridized on a chip to determine expression. The set of enriched differentially expressed miRNAs was analyzed by gene ontology and the Kyoto Encyclopedia of Genes and Genomes to describe the functional properties of the key biological processes and pathways. We conducted a bioinformatics analysis using Cytoscape to elucidate the interactions between miRNAs and proteins. RESULTS: We found that the expression of 186 lncRNAs was significantly different in the model of chondrocyte degeneration, in which 88 lncRNAs were upregulated, and 98 were downregulated. Expression of 684 miRNAs was significantly different. Analysis of the protein–protein interaction (PPI) network indicated that the genes for CXCL10, ISG15, MYC, MX1, OASL, IFIT1, RSAD2, MX2, IFI44L, and BST2 are the top 10 core genes, identifying the most important functional modules to elucidate the differential expression of miRNAs. CONCLUSIONS: These data may provide new insights into the molecular mechanisms of chondrocyte degeneration in osteoarthritis, and the identification of lncRNAs and miRNAs may provide potential targets for the differential diagnosis and therapy of osteoarthritis. Sciendo 2022-08-31 /pmc/articles/PMC10321185/ /pubmed/37551168 http://dx.doi.org/10.2478/abm-2022-0021 Text en © 2022 Guoliang Wang et al., published by Sciendo https://creativecommons.org/licenses/by/4.0/This work is licensed under the Creative Commons Attribution 4.0 International License.
spellingShingle Original Article
Wang, Guoliang
He, Lu
Xiang, Yaoyu
Jia, Di
Li, Yanlin
Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title_full Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title_fullStr Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title_full_unstemmed Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title_short Long noncoding and micro-RNA expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
title_sort long noncoding and micro-rna expression in a model of articular chondrocyte degeneration induced by stromal cell-derived factor-1
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10321185/
https://www.ncbi.nlm.nih.gov/pubmed/37551168
http://dx.doi.org/10.2478/abm-2022-0021
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