ArticleJournal of nanobiotechnology2023
Plasma exosome miRNA-26b-3p derived from idiopathic short stature impairs longitudinal bone growth via the AKAP2/ERK1/2 axis.
Article in Journal of nanobiotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.
- Charting the growth of idiopathic short stature research: a 32-year bibliometric study of global advances.Frontiers in endocrinology · 2025Pooled it
- The exosomal miR-26b-3p derived from Crohn's disease-associated mesenteric adipose tissue induces M1 macrophage polarization and exacerbates ileocolonic anastomosis inflammation via the p38-MAPK signaling pathway.Frontiers in immunology · 2026Article
- Emerging molecular mechanisms of the ECM-exosome growth-plate axis in idiopathic short stature.Frontiers in cell and developmental biology · 2026Review
- Capsaicin diet drives gut inflammation and exosomal miR-17-3p elevation in idiopathic short stature.Nature communications · 2025Article
- Characterization of microRNA and Metabolite Profiles of Seminal Extracellular Vesicles in Boars.Animals : an open access journal from MDPI · 2025Article
- Cardioprotective effects of hUCMSCs-Exosi-EGR1 MN patch in MI/RI by modulating oxidative stress and mitophagy.Materials today. Bio · 2025Article
- Exploring the molecular interface of gene expression dynamics and prostate cancer susceptibility in response to HBCD exposure.Toxicology research · 2025Article
- Non-invasive biomarkers for brain aging: the role of autophagy-related microRNAs in plasma exosomes.Frontiers in molecular neuroscience · 2025Article
- miRNA-based regulation in growth plate cartilage: mechanisms, targets, and therapeutic potential.Frontiers in endocrinology · 2025Review
- Plasma exosomes from patients with active thyroid-associated orbitopathy induce inflammation and fibrosis in orbital fibroblasts.Journal of translational medicine · 2024Article
- Epithelial cells derived exosomal miR-203a-3p facilitates stromal inflammation of type IIIA chronic prostatitis/chronic pelvic pain syndrome by targeting DUSP5 and increasing MCP-1 generation.Journal of nanobiotechnology · 2024Article
- [Growth plate regulation and short stature: mechanistic insights and therapeutic advances].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatricsReview
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6 authors at 1 institution in 1 country.
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Abstract
backgroundCurrently, 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.
methodsThe 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.
resultsChondrocytes proliferation and endochondral ossification were suppressed after coculture of ISS plasma exosomes with human normal chondrocytes. High-throughput microRNA sequencing and RT-qPCR confirmed that plasma exosome miR-26b-3p was upregulated in ISS children. Meanwhile, exosome miRNA-26b-3p showed a high specificity and sensitivity in discriminating ISS from normal children. The rescue experiment showed that downregulation of miR-26b-3p obviously improved the repression of chondrocyte proliferation and endochondral ossification caused by ISS exosomes. Subsequently, miR-26b-3p overexpression inhibited chondrocyte proliferation and endochondral ossification once again. In situ hybridization confirmed the colocalization of miR-26b-3p with AKAP2 in chondrocytes. In vitro and in vivo assay revealed exosome miRNA-26b-3p impairs longitudinal bone growth via the AKAP2 /ERK1/2 axis.
conclusionsThis study is the first to confirm that miR-26b-3p overexpression in ISS plasma exosomes leads to disorders in proliferation and endochondral ossification of growth plate cartilage via inhibition of AKAP2/ERK1/2 axis, thereby inducing ISS. This study provides a new research direction for the etiology and pathology of ISS and a new idea for the biological treatment of ISS.
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