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http://purl.uniprot.org/citations/29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/29323718http://www.w3.org/2000/01/rdf-schema#comment"The study aimed to investigate the impact of miR-182 and FOXO1 on S. japonica-induced hepatic fibrosis. Microarray analysis was performed to screen out differential expressed miRNAs and mRNAs. Rat hepatic fibrosis model and human hepatocellular cell line LX-2 were used to study the effect of miR-182 and FOXO1. qRT-PCR and Western blot were used to detect the expression of miR-182, FOXO1 or other fibrosis markers. The targeting relationship between FOXO1 and miR-182 was verified by luciferase reporter assay. Immunohistochemistry or immunofluorescence staining was conducted to detect FOXO1 or α-SMA in rat hepatic tissues. Cell viability and apoptosis were detected by MTT assay and flow cytometry. The expression of PI3K/AKT pathway-related proteins was detected by Western blot. miR-182 was highly expressed in liver fibrosis samples, and FOXO1 expression was negatively correlated with miR-182 expression. After transfection of miR-182, FOXO1 expression was down-regulated, with the results of LX-2 cells proliferation inhibition and apoptosis induction, as well as the aggravation of rat hepatic fibrosis. The expression of p-AKT/AKT and p-S6/S6 was increased, meaning that the PI3K/AKT signal pathway was activated. The results were reversed when treated with Wortmannin (PI3K inhibitor). After transfection of miR-182 inhibitor, FOXO1 expression was up-regulated, LX-2 cell proliferation was inhibited, and apoptosis rate was increased. High-expressed miR-182 and low-expressed FOXO1 promoted proliferation and inhibiting apoptosis on liver fibrosis cells, stimulating the development of S. japonica-induced hepatic fibrosis through feeding back to PI3K/AKT signaling pathway."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.org/dc/terms/identifier"doi:10.1002/jcp.26469"xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Fan X."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Kong H."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Huang Y."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Huang J."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Song Q."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Zhang H."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Wang L."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/author"Tao R."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/name"J Cell Physiol"xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/pages"6693-6704"xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/title"Effect of miR-182 on hepatic fibrosis induced by Schistosomiasis japonica by targeting FOXO1 through PI3K/AKT signaling pathway."xsd:string
http://purl.uniprot.org/citations/29323718http://purl.uniprot.org/core/volume"233"xsd:string
http://purl.uniprot.org/citations/29323718http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/29323718
http://purl.uniprot.org/citations/29323718http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/29323718
http://purl.uniprot.org/uniprot/#_A0A0G2K4M6-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_D3ZFJ0-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_A0A1W2Q6C8-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_A0A8I6AKZ7-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_A0A8I6G230-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_A0A8I6GKP1-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718
http://purl.uniprot.org/uniprot/#_A1E251-mappedCitation-29323718http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/29323718