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Identification of the key gene and pathways associated with osteoarthritis via single-cell RNA sequencing on synovial fibroblasts
Osteoarthritis (OA) is a chronic degenerative joint disease with its onset closely related to the growth of synovial fibroblasts (SFs), yet the genes involved in are few reported. In our study, we aimed to identify the OA-associated key gene and pathways via the single-cell RNA sequencing (scRNA-seq...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Lippincott Williams & Wilkins
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7437759/ https://www.ncbi.nlm.nih.gov/pubmed/32872047 http://dx.doi.org/10.1097/MD.0000000000021707 |
Sumario: | Osteoarthritis (OA) is a chronic degenerative joint disease with its onset closely related to the growth of synovial fibroblasts (SFs), yet the genes involved in are few reported. In our study, we aimed to identify the OA-associated key gene and pathways via the single-cell RNA sequencing (scRNA-seq) analysis on SFs. scRNA-seq data of SFs from OA sufferers were accessed from GEO database, then the genes involved in were subjected to principal component analysis (PCA) and T-Stochastic Neighbor Embedding (TSNE) Analysis. GO and KEGG enrichment analyses were performed to find the most enriched functions and pathways associated with marker genes and a PPI network was constructed to identify the key gene associated with OA occurrence. Findings revealed that marker genes in three cell types identified by TSNE were mainly activated in pathways firmly related to fibroblasts growth, such as extracellular matrix, immune and cell adhesion molecule binding-associated functions and pathways. Moreover, fibronectin1 (FN1) was validated as the key gene that was tightly related to the growth of SFs, as well as had the potential to play a key role in OA occurrence. Our study explored the key gene and pathways associated with OA occurrence, which were of great value in further investigation of OA diagnosis as well as pathogenesis. |
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