BackgroundAlzheimer's disease (AD) is a progressive neurodegenerative disease characterized by complex pathobiological characteristics and still lacks accurate biomarkers in early diagnosis. Neuritin (NRN1) is a neurotrophic factor, which has active roles in neuronal plasticity and regeneration. Recent research suggests that Neuritin has been associated with loss of cognitive function, maybe a potential therapeutic target in AD. MethodsWe have clustered the upregulated miRNAs in AD and predicted the target miRNAs of Neuritin by bioinformatics analysis, found miR-188-5p may involve in the development of AD. ResultsIn the present study, we confirm the association between Neuritin and miR-188-5p expression in mice with AD. Besides, we provide evidence for the changes of cognition capacity, miR-188-5p and Neuritin levels in APP/PS1 mice. ConclusionOur results reveal a previously undefined mechanism that miR-188-5p plays a significant role in the development of AD by inhibiting the expression of target protein Neuritin.
Background Age-related hearing loss (ARHL) is the most common sensory deficit and refers to the gradual loss of hearing function with age. We aimed to research the differential expression genes during the occur of ARHL and explore microRNAs that maybe regulate these genes. Methods Search the GEO data GSE6045, GSE35234, GSE62173, GSE45026 from NCBI's Gene Expression Omnibus database, and analyze in R. Normalize GEO data by RMA method in R, and use linear microarray data model (LIMMA) method in R to compare young and old mice to find differential genes and microRNAs. Results 109 up-regulated and 121 down-regulated important genes were identified respectively. Functional enrichment shows that they are significantly enriched in protein digestion and absorption, neuroactive ligand-receptor interaction, and PI3K-Akt signaling pathway. Among the top 20 Hub genes, 7 down-regulated genes (Col3a1, Col1a2, Sparc, Col4a2, Col2a1, Lox, Sparc, Ctgf) have verified targeted miRNAs, which have interaction with differential miRNAs of GSE45026. Finally, we designated miR-29a-3p, miR-29b-3p, miR-29c-3p, and miR-124-3p as key miRNAs involved in the development of age-related hearing loss. Conclusions These low expression genes of Col3a1, Col1a2, Sparc, Col4a2, Col2a1,Lox, Sparc, and Ctgf maybe key genes of ARHL, and probably regulated by miR-29a-3p, miR-29b-3p, miR-29c-3p, and miR-124-3p.
Objective Hearing loss is a common neurodegenerative disease and few studies on miRNAs associated with hearing loss. This study screened the differentially expressed miRNAs in hearing loss and explored the relationship between Neuritin and hearing loss at the same time. Methods The combination of kanamycin sulfate and furosemide was used to establish a mouse hearing loss model. High-throughput sequencing was used to screen the differentially expressed miRNAs during hearing loss. ABR was used to detect listening function. QRT-PCR was used to identify the expression of differential miRNAs in hearing loss. Western blot was used to detect the expression of Neuritin protein. Luciferase was used to identify the binding sites of miRNA and Neuritin. Results Neuritin expression decreases after hearing loss. 24 up-regulated miRNAs and 66 down-regulated miRNAs were screened by sequencing. The expression of miR-224-5p increased in the Corti after hearing loss (p < 0.05). MiR-224-5p can inhibit expression of Neuritin and specifically bind to neuritin gene (p < 0.05). Conclusion Up-regulated miRNA-224-5p in hearing loss can target the expression of Neuritin.
Objective: This study screened the differentially expressed miRNAs in the mouse cochlea during hearing loss and explored the relationship between miR-224-5p and Neuritin.Methods: The combination of kanamycin sulfate and furosemide was used to establish a mouse hearing loss model. High-throughput sequencing was used to screen the differentially expressed miRNAs during hearing loss. qRT-PCR was used to identify the expression of differential miRNAs in hearing loss. Western Blot was used to detect the expression of Neuritin protein. Luciferase was used to identify the binding site of miRNA and Neuritin.Results: The expression of miR-224-5p in the mouse cochlea increased during hearing loss (p<0.05). MiR-224-5p mimics can reduce Neuritin protein expression in 293T cells (p<0.05). MiR-224-5p can specifically bind to Neuritin (p<0.05).Conclusion: The expression of miR-224-5p increases in hearing loss and targets the expression of Neuritin
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