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TL;DR
The study used high-throughput sequencing to identify differentially expressed miRNAs in plasma exosomes from children with ISS versus normal controls.
Journal of Nanobiotechnology · 6 authors, 3 centres
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The study used high-throughput sequencing to identify differentially expressed miRNAs in plasma exosomes from children with ISS versus normal controls.
The study used high-throughput sequencing to identify differentially expressed miRNAs in plasma exosomes from children with ISS versus normal controls. It found miR-26b-3p was upregulated in ISS exosomes. In vitro, co-culturing these exosomes with normal human chondrocytes suppressed cell proliferation and endochondral ossification; downregulating miR-26b-3p rescued this effect. In vivo, overexpressing miR-26b-3p in rats via exosomes or adenovirus impaired growth plate cartilage development. Mechanistically, miR-26b-3p directly targeted AKAP2, reducing its expression and the phosphorylation of ERK1/2.