Cargando…
Identification of the Core MicroRNAs and Potential Molecular Mechanismsin Sarcoidosis Using Bioinformatics Analysis
Sarcoidosis is a systemic heterogeneous inflammatory disease; however, the etiology and pathogenesis of sarcoidosis are still unknown. Herein, we investigated the core microRNAs and potential molecular mechanisms in sarcoidosis. The DE-miRNAs were diagnosed using the LIMMA software package. DIANA-mi...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2021
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8155597/ https://www.ncbi.nlm.nih.gov/pubmed/34055877 http://dx.doi.org/10.3389/fmolb.2021.644232 |
Sumario: | Sarcoidosis is a systemic heterogeneous inflammatory disease; however, the etiology and pathogenesis of sarcoidosis are still unknown. Herein, we investigated the core microRNAs and potential molecular mechanisms in sarcoidosis. The DE-miRNAs were diagnosed using the LIMMA software package. DIANA-mirPath was employed to perform pathway and GO enrichment analysis of the DE-miRNAs. PPI networks and miRNA-target gene regulatory networks were used to obtain insight into the actions of DE-miRNAs. Expression of the hub genes along with miRNAs was validated in clinical specimens. Overall, 266 DE-miRNAs were screened. Among these DE-miRNAs, hsa-miR-144, hsa-miR-126, as well as hsa-miR-106a were the upmost upregulated miRNAs; hsa-miR-151-3p, hsa-miR-320d, and hsa-miR-324-3p were the top downregulated miRNAs. NR3C1, ZBTB7A, NUFIP2, BZW1, ERGIC2, and VEGFA were mapped as the most targeted hub genes in the upregulation of miRNAs, and MCL1 and SAE1 were the most targeted hub genes in the downregulation of miRNA. VEGFA and NR3C1 were selected and potentially modulated by hsa-miR-20b, hsa-miR-126, and hsa-miR-106a. In sarcoidosis pathological tissue, hsa-miR-126 was highly expressed, and VEGFA and NR3C1 were overexpressed. In conclusion, our results revealed the dysregulation of hsa-miR-126 and a potential regulatory mechanism for pathogenesis in sarcoidosis. |
---|