MiR-29a-3p coordinates the ECM-integrin-adaptor protein axis to regulate focal adhesion in allergic rhinitis [RNA-Seq]
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PROVIDER: PRJNA1037075 | ENA |
REPOSITORIES: ENA
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Project description: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.
2024-10-01 | GSE247294 | GEO
Project description: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.
2024-10-01 | GSE247293 | GEO
Project description:miR-29a-3p coordinates the ECM-integrin-adaptor protein axis to regulate focal adhesion in allergic rhinitis
| PRJNA1037068 | ENA
Project description:miR-29a-3p coordinates the ECM-integrin-adaptor protein axis to regulate focal adhesion in allergic rhinitis [miRNA-Seq]
| PRJNA1037074 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-10-01 | GSE247295 | GEO
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been obserbed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis.
2015-03-31 | E-GEOD-67423 | biostudies-arrayexpress
Project description:To confirm the mechanism of miR-29a in liver fibrosis healing, we have employed whole genome microarray expression profiling as a discovery platform to identify genes. CCl4 and TAA liver fibrosis model mouse were used for this experiment. After five weeks liver fibrosis induction period, mouse have been observed for one week (1w) or two weeks (2w) and negative control nucleotide (N.C) or miR-29a were injected every 3 days on this period. We used CCl4 1w N.C (n = 1), 1w miR-29a (n = 1), 2w N.C (n = 1), 2w miR-29a (n = 1), and also used TAA model mouse (total n = 8) liver samples for microarray analysis. We can get only one gene (PDGF-c) as a target of miR-29a which relate to liver fibrosis and down-regulated more than 1.5 times in common miR-29a injected group than N.C group.
2015-03-31 | GSE67423 | GEO
Project description:miR-29a/b1 was reported to be involved in the regulation of reproductive function in female mice, but the underlying molecular mechanisms were not clear. In this study, female mice lacking miR-29a/b1 showed a delay in vaginal opening, irregular estrus cycles, ovulation disorder and infertility. However, the development of egg was normal in mutant mice and the ovulation disorder could be rescued by the superovulation treatment. The plasma level of luteinizing hormone (LH) was significantly lower in the mutant mice. Using iTRAQ coupled with LC-MS/MS, we found that the deficiency of miR-29a/b1 in mice resulted in an abnormal expression of a number of proteins involved in vesicular transport and secretion in the pituitary gland. The miR-29a/b1 targeting gene Dnmt3a and Hdac4 were up-regulated in the pituitary of miR-29a/b1 knockout mice suggesting that these two epigenetic writers may be the upstream causes for these phenotype changes due to miR-29a/b1 deficiency. These findings demonstrated that miR-29a/b1 is indispensable for the function of the reproductive axis through regulating LH secretion in the pituitary gland.
2021-09-09 | PXD017106 | Pride
Project description:Activation of the Wnt pathway is at the core of many human cancers. During canonical Wnt signaling, the Lrp6 and Frizzled receptors bind to the Wnt growth factor, which leads to the complex being endocytosed. Glycogen Synthase Kinase 3 (GSK3), Dishevelled (Dvl), and Axin are sequestered inside the intraluminal vesicles of late endosomes, known as multivesicular bodies (MVBs). Here we present experiments showing that Wnt causes the endocytosis of focal adhesion (FA) proteins and depletion of Integrin β 1 (ITGβ1) from the cell surface. FAs and integrins provide link the cytoskeleton to the extracellular matrix. Wnt-induced macropinocytosis of the plasma membrane caused ITGβ1 depletion and was accompanied by striking changes in the actin cytoskeleton. In situ protease protection assays in cultured cells showed that ITGβ1 was sequestered within membrane-bounded organelles that corresponded to Wnt-induced MVBs containing GSK3 and focal adhesion-associated proteins. An in vivo model using Xenopus embryos dorsalized by Wnt8 mRNA showed that ITGβ1 depletion decreased Wnt signaling. The cross-talk between Wnt signaling, membrane trafficking, and focal adhesions should be relevant to human cancer and cell biology.
2022-03-18 | GSE193381 | GEO