MiR-29a-3p coordinates the ECM-integrin-adaptor protein axis to regulate focal adhesion in allergic rhinitis [RNA-Seq]
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ABSTRACT: MiR-29a-3p plays a crucial role in regulating cell-cell junctions in the nasal mucosa epithelial cells of individuals with allergic rhinitis (AR). However, the impact of miR-29a-3p on focal adhesion (FA) homeostasis or cell-extracellular matrix (ECM) adhesion remains uncertain. This study demonstrates that miR-29a-3p can regulate the expression of LAMC1 and ITGA6, showing a potential correlation with AR pathogenesis in humans. Furthermore, the targeted inhibitory relationship between miR-29a-3p and both LAMC1 and ITGA6 was confirmed through dual-luciferase reporter assays. Analysis of miRNA-seq and mRNA-seq datasets established a differential expression (DE) profile for AR-associated genes, revealing 278 DE-miRNAs and 11,352 DE-mRNAs. Based on this data, we assert that miR-29s are a remarkable example of a single microRNA family exhibiting a consistent upregulation trend in AR. The KEGG analysis showed that AR is significantly associated with FA and ECM-receptor interaction. By integrating online databases for miRNA-target prediction with mRNA-seq data, we identified crucial genes involved in FA (e.g., ITGA6) and cell-ECM adhesion (e.g., LAMC1) as potential targets of miR-29s. Consequently, the role of the entire miRNA transcriptome can be virtually encompassed by miR-29s. In vivo evidence from AR mouse models further supported the role of miR-29a-3p in repressing these proteins' expression. Our findings provide a comprehensive understanding of the significant differential expression of miRNA/mRNA genes in AR, with a specific focus on miR-29a-3p. This particular miRNA appears to hinder the process of FA and cell-ECM adhesion by targeting the ECM-integrins-adaptor protein axis, potentially contributing to the pathogenesis of AR.
ORGANISM(S): Mus musculus
PROVIDER: GSE247293 | GEO | 2024/10/01
REPOSITORIES: GEO
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