<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liu X</submitter><funding>the National Nature Science Foundation of China</funding><funding>The National Nature Science Foundation of China</funding><pagination>94</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10022307</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>21(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>Chondrocyt</pubmed_abstract><journal>Journal of nanobiotechnology</journal><pubmed_title>Plasma exosome miRNA-26b-3p derived from idiopathic short stature impairs longitudinal bone growth via the AKAP2/ERK1/2 axis.</pubmed_title><pmcid>PMC10022307</pmcid><funding_grant_id>81960392</funding_grant_id><funding_grant_id>82060169</funding_grant_id><pubmed_authors>Liu X</pubmed_authors><pubmed_authors>Wu Z</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Shen Y</pubmed_authors><pubmed_authors>Yuan J</pubmed_authors><pubmed_authors>Jia J</pubmed_authors></additional><is_claimable>false</is_claimable><name>Plasma exosome miRNA-26b-3p derived from idiopathic short stature impairs longitudinal bone growth via the AKAP2/ERK1/2 axis.</name><description>&lt;h4>Background&lt;/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.&lt;h4>Methods&lt;/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.&lt;h4>Results&lt;/h4>Chondrocyt</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Mar</publication><modification>2025-04-22T18:24:57.549Z</modification><creation>2025-04-06T02:24:30.328Z</creation></dates><accession>S-EPMC10022307</accession><cross_references><pubmed>36927779</pubmed><doi>10.1186/s12951-023-01849-8</doi></cross_references></HashMap>