RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/38129425http://www.w3.org/2000/01/rdf-schema#comment"Clinical studies have found 14-3-3η to be associated with osteoporosis through undefined mechanisms. We aimed to investigate the role of 14-3-3η in osteoporosis and its potential associations with miRNAs. The Gene Expression Omnibus(GEO) and Human Protein Atlas 1 databases were analyzed to examine both the mRNA and protein expression of 14-3-3η in OP. Gene enrichment analyses were performed to explore the underlying mechanism of 14-3-3η based on DAVID. miRWalk was used to predict the associated miRNAs. The statistics were analysed by R software and SPSS software. 14-3-3η was overexpressed and knock down expressed in BMSCs by lentiviral vector transfecting. And BMSCs were induced by hypoxia. qRT-PCR and Western-Blot verified the expression of mRNA and protein. Scratch assay detected the migration of osteocytes. Co-immunoprecipitation and luciferase assay studied the 14-3-3η targeted protein and miRNA. overexpression and knock down of miRNA to verify the relationship of 14-3-3η and target genes. The 14-3-3η mRNA expression level was low in patients with osteoporosis, as corroborated by immunohistochemical staining images. Functional analyses revealed enrichment of the MAPK-associated cascade. 14-3-3η was correlated with MAPK family proteins and five key miRNAs, including mir-142-3p. In addition, 14-3-3η knockdown in BMSCs increased the mRNA and protein expression levels of Hif-α, VEGF, BMP-2, OPN, OST, and Runx2, and enhanced the cells migration ability. Under hypoxic conditions, Hif-α and BMP-2 protein expression levels were upregulated, whereas those of 14-3-3η and MAPK3 were downregulated. Co-immunoprecipitation experiments showed decreased binding of 14-3-3η to MAPK3. 14-3-3η knockdown produced the same results as hypoxia induction. Adding caspase3 inhibitor and knocking down 14-3-3η again prevented MAPK3 cleavage by caspase3 and inhibited BMP-2 expression. Moreover, under hypoxic conditions, miR-142-3P expression was upregulated and luciferase assays revealed 14-3-3η as its target gene. miR-142-3P overexpression decreased mRNA and protein levels of 14-3-3η and MAPK3, while increasing BMP-2 expression. miR-142-3P knockdown reversed these results. BMSC osteogenesis was suppressed by 14-3-3η, whereas miRNA-142-3p promoted it through the inhibition of 14-3-3η."xsd:string
http://purl.uniprot.org/citations/38129425http://purl.org/dc/terms/identifier"doi:10.1038/s41598-023-48950-4"xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/author"Liu Y.Q."xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/author"Xu Y.C."xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/author"Shuai Z.W."xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/date"2023"xsd:gYear
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/name"Sci Rep"xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/pages"22862"xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/title"Mir-142-3P regulates MAPK protein family by inhibiting 14-3-3eta to enhance bone marrow mesenchymal stem cells osteogenesis."xsd:string
http://purl.uniprot.org/citations/38129425http://purl.uniprot.org/core/volume"13"xsd:string
http://purl.uniprot.org/citations/38129425http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/38129425
http://purl.uniprot.org/citations/38129425http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/38129425
http://purl.uniprot.org/uniprot/#_A1QJE5-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_B2R6N6-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_L7RXH5-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_P27361-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_Q04917-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_Q9H4N8-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_Q7Z3H5-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_Q8NHX0-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/#_Q9BWJ1-mappedCitation-38129425http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/Q8NHX0http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/Q9H4N8http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/38129425
http://purl.uniprot.org/uniprot/P27361http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/38129425