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Updated: Sep 1, 2025
Isolating, Sequencing and Analyzing Extracellular MicroRNAs from Human Mesenchymal Stem Cells
Published on: March 8, 2019
microRNA-93 packaged in extracellular vesicles from mesenchymal stem cells reduce neonatal hypoxic-ischemic brain
Hongcheng Luo1, Fugao Huang2, Zhijing Huang3
1Department of Medical Laboratory, Affiliated Hospital of Youjiang Medical University for Nationalities, Baise 533000, Guangxi, China; Medical College of Guangxi University, Nanning 530004, Guangxi, China.
Objective:
Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) have been proposed as a promising strategy for treating ischemia-related diseases. Herein, we probed into the role of miR-93 delivered by BMSC-EVs in hypoxic-ischemic brain injury (HIBD).
Methods:
Neonatal HIBD mouse models and hippocampal neuron models of oxygen glucose deprivation (OGD) were constructed. EVs were isolated from the culture medium of bone marrow MSCs (BMSCs). After co-culture of BMSC-EVs with OGD-exposed hippocampal neurons, the effect of microRNA-93 (miR-93) delivered by BMSC-EVs on OGD-induced hippocampal neurons as well as on HIBD in vivo under transfection of miR-93 mimic or inhibitor was explored. The interaction among miR-93, JMJD3, and p53/KLF2 axis was assessed.
Results:
BMSC-EVs prevented OGD-induced hippocampal neuron apoptosis and inflammation, which was associated with their transfer of miR-93 into the hippocampal neurons. miR-93 targeted JMJD3 and downregulated its expression, thus inhibiting the OGD-induced hippocampal neuron apoptosis. By regulating the JMJD3/p53/KLF2 axis, miR-93 in BMSC-EVs reduced the OGD-induced hippocampal neuron apoptosis in vitro as well as alleviating HIBD in vivo.
Conclusions:
The current study highlighted that miR-93 delivered by BMSC-EVs alleviated HIBD in neonatal mice through the JMJD3-dependent p53/KLF2 axis.
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