Journal
CELL DEATH & DISEASE
Volume 13, Issue 3, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41419-022-04703-1
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Funding
- National Natural Science Foundation of China [82000701]
- Beijing Municipal Administration of Hospitals Clinical Medicine Development of Special Funding Support [ZYLX201824]
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This study demonstrates that bone marrow mesenchymal stem cell-derived exosomes play a role in alleviating vascular calcification by inhibiting cellular apoptosis through the delivery of enclosed miR-381-3p, which targets NFAT5 mRNA. The findings contribute to a better understanding of the mechanism of chronic kidney disease-related vascular calcification.
Vascular calcification (VC) is a significant complication of chronic kidney disease (CKD) and cellular apoptosis is one of the intricate mechanisms of VC. Bone marrow mesenchymal stem cell-derived exosome (BMSC-Exo) alleviates VC, but the mechanism remains unclear. We investigated the mechanism of BMSC-Exo using high phosphate stimulated Human aortic smooth muscle cells (HA-VSMCs) and 5/6 subtotal nephrectomy (SNx) rat models. We demonstrated that the effect of BMSC-Exo on the inhibition of cellular apoptosis and calcification partially depended on exosomal microRNA-381-3p (miR-381-3p) both in vivo and in vitro, and confirmed that miR-381-3p could inhibit Nuclear Factor of Activated T cells 5 (NFAT5) expression by directly binding to its 3' untranslated region. Additionally, we found that severe calcification of arteries in dialysis patients was associated with decreased miR-381-3p and increased NFAT5 expression levels. Collectively, our findings proved that BMSC-Exo plays anti-calcification and anti-apoptosis roles in CKD by delivering enclosed miR-381-3p, which directly targets NFAT5 mRNA, and leads to a better understanding of the mechanism of CKD-VC.
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