{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu X"],"funding":["the National Nature Science Foundation of China","The National Nature Science Foundation of China"],"pagination":["94"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10022307"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["21(1)"],"pubmed_abstract":["<h4>Background</h4>Currently, the etiology of idiopathic short stature (ISS) is still unclear. The poor understanding of the molecular mechanisms of ISS has largely restricted this strategy towards safe and effective clinical therapies.<h4>Methods</h4>The plasma exosomes of ISS children were co-cultured with normal human chondrocytes. The differential expression of exosome miRNA between ISS and normal children was identified via high-throughput microRNA sequencing and bioinformatics analysis. Immunohistochemistry, In situ hybridization, RT-qPCR, western blotting, luciferase expression, and gene overexpression and knockdown were performed to reveal the key signaling pathways that exosome miRNA of aberrant expression in ISS children impairs longitudinal bone growth.<h4>Results</h4>Chondrocyt"],"journal":["Journal of nanobiotechnology"],"pubmed_title":["Plasma exosome miRNA-26b-3p derived from idiopathic short stature impairs longitudinal bone growth via the AKAP2/ERK1/2 axis."],"pmcid":["PMC10022307"],"funding_grant_id":["81960392","82060169"],"pubmed_authors":["Liu X","Wu Z","Zhang J","Shen Y","Yuan J","Jia J"],"additional_accession":[]},"is_claimable":false,"name":"Plasma exosome miRNA-26b-3p derived from idiopathic short stature impairs longitudinal bone growth via the AKAP2/ERK1/2 axis.","description":"<h4>Background</h4>Currently, the etiology of idiopathic short stature (ISS) is still unclear. The poor understanding of the molecular mechanisms of ISS has largely restricted this strategy towards safe and effective clinical therapies.<h4>Methods</h4>The plasma exosomes of ISS children were co-cultured with normal human chondrocytes. The differential expression of exosome miRNA between ISS and normal children was identified via high-throughput microRNA sequencing and bioinformatics analysis. Immunohistochemistry, In situ hybridization, RT-qPCR, western blotting, luciferase expression, and gene overexpression and knockdown were performed to reveal the key signaling pathways that exosome miRNA of aberrant expression in ISS children impairs longitudinal bone growth.<h4>Results</h4>Chondrocyt","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Mar","modification":"2025-04-22T18:24:57.549Z","creation":"2025-04-06T02:24:30.328Z"},"accession":"S-EPMC10022307","cross_references":{"pubmed":["36927779"],"doi":["10.1186/s12951-023-01849-8"]}}